origin and evolution of transporter substrate specificity within the npf family
morten egevang jørgensen, deyang xu, christoph crocoll, david ramírez, mohammed saddik motawia, carl erik olsen, hussam hassan nour-eldin, barbara ann halkier 2017
Despite vast diversity in metabolites and the matching substrate specificity of their transporters, little is known about how evolution of transporter substrate specificities is linked to emergence of substrates via evolution of biosynthetic pathways. Transporter specificity towards the recently evolved glucosinolates characteristic of Brassicales is shown to evolve prior to emergence of glucosinolate biosynthesis. Furthermore, we show that glucosinolate transporters belonging to the ubiquitous NRT1/PTR FAMILY (NPF) likely evolved from transporters of the ancestral cyanogenic glucosides found across more than 2500 species outside of the Brassicales. Biochemical characterization of orthologs along the phylogenetic lineage from cassava to A. thaliana, suggests that alterations in the electrogenicity of the transporters accompanied changes in substrate specificity. Linking the evolutionary path of transporter substrate specificities to that of the biosynthetic pathways, exemplify how transporter substrate specificities originate and evolve as new biosynthesis pathways emerge.
All living cells are surrounded by membranes that protect them from the external environment. The membrane contains proteins called transporters, which move nutrients and other molecules (known as substrates) across the membrane. A variety of transporters have evolved to move the hundreds of thousands of different substrates found in nature.
Plant cells make many different compounds to protect themselves from pests and diseases. A group of transporters known as the NPF family move some of these compounds across the cells outer membrane. The types of substrates they transport vary in different plants. In cassava, for example, NPF transporters move compounds called cyanogenic glucosides, which are poisonous to humans and other animals. On the other hand, NPF transporters in another plant called Arabidopsis thaliana can move bitter-tasting compounds called glucosinolates. The process that makes glucosinolates in plants evolved from the process that makes cyanogenic glucosides.
Can transporters evolve the ability to move a new substrate before or after that substrate first appears? To answer this question, Jørgensen et al. studied the NPF family in A. thaliana, cassava and another plant called papaya that makes both cyanogenic glucosides and glucosinolates. The experiments suggest that NPF transporters able to move both cyanogenic glucosides and glucosinolates evolved before plants evolved the ability to make glucosinolates. Later in evolution, these multi-specific transporters specialized to only move glucosinolates. Jørgensen et al. also show that early glucosinolate transporters could move a broad variety of glucosinolates but later evolved to only transport particular types.
These findings show how transporters and the processes that make compounds in cells may evolve together. A future challenge will be to understand the molecular changes in a transporter that make it specific for a certain substrate. This may help researchers to develop new ways of controlling the amount of toxic compounds in crops we eat by manipulating how the compounds are transported.
environmental change explains cichlid adaptive radiation at lake malawi over the past 1.2 million years
sarah j. ivory, margaret w. blome, john w. king, michael m. mcglue, julia e. cole, andrew s. cohen 2016
Tropical African lakes are well-known to house exceptionally biodiverse assemblages of fish and other aquatic fauna, which are thought to be at risk in the future. Although the modern assemblages are well-studied, direct evidence of the origin of this incredible wealth of species and the mechanisms that drive speciation are virtually unknown. We use a long sedimentary record from Lake Malawi to show that over the last 1.2 My both large-scale climatic and tectonic changes resulted in wet–dry transitions that led to extraordinary habitat variability and rapid diversification events. This work allows us to understand the environmental context of aquatic evolution in the most biodiverse tropical lake.
Long paleoecological records are critical for understanding evolutionary responses to environmental forcing and unparalleled tools for elucidating the mechanisms that lead to the development of regions of high biodiversity. We use a 1.2-My record from Lake Malawi, a textbook example of biological diversification, to document how climate and tectonics have driven ecosystem and evolutionary dynamics. Before ∼800 ka, Lake Malawi was much shallower than today, with higher frequency but much lower amplitude water-level and oxygenation changes. Since ∼800 ka, the lake has experienced much larger environmental fluctuations, best explained by a punctuated, tectonically driven rise in its outlet location and level. Following the reorganization of the basin, a change in the pacing of hydroclimate variability associated with the Mid-Pleistocene Transition resulted in hydrologic change dominated by precession rather than the high-latitude teleconnections recorded elsewhere. During this time, extended, deep lake phases have abruptly alternated with times of extreme aridity and ecosystem variability. Repeated crossings of hydroclimatic thresholds within the lake system were critical for establishing the rhythm of diversification, hybridization, and extinction that dominate the modern system. The chronology of these changes closely matches both the timing and pattern of phylogenetic history inferred independently for the lake’s extraordinary array of cichlid fish species, suggesting a direct link between environmental and evolutionary dynamics.
diverse non-genetic, allele-specific expression effects shape genetic architecture at the cellular level in the mammalian brain
wei-chao huang et al. 2017
•In vivo genome-wide screen uncovers diverse non-genetic allelic effects
•Non-genetic allelic effects are prevalent in the neonatal mouse brain
•Allelic effects cause mosaics of mutant and wild-type cells for heterozygous mutations
•Allelic effects exist in the primate brain and impact genes linked to mental illness
Interactions between genetic and epigenetic effects shape brain function, behavior, and the risk for mental illness. Random X inactivation and genomic imprinting are epigenetic allelic effects that are well known to influence genetic architecture and disease risk. Less is known about the nature, prevalence, and conservation of other potential epigenetic allelic effects in vivo in the mouse and primate brain. Here we devise genomics, in situ hybridization, and mouse genetics strategies to uncover diverse allelic effects in the brain that are not caused by imprinting or genetic variation. We found allelic effects that are developmental stage and cell type specific, that are prevalent in the neonatal brain, and that cause mosaics of monoallelic brain cells that differentially express wild-type and mutant alleles for heterozygous mutations. Finally, we show that diverse non-genetic allelic effects that impact mental illness risk genes exist in the macaque and human brain. Our findings have potential implications for mammalian brain genetics.
“silencing one gene copy may be a way in which cells fine tune their genetic program at specific times during the lifecycle of the animal, or in discrete places”
impacts of neanderthal-introgressed sequences on the landscape of human gene expression
rajiv c. mccoy, jon wakefield, joshua m. akey 2017
trade-off between transcriptome plasticity and genome evolution in cephalopods
liscovitch-brauer et al. 2017
•Unlike other taxa, cephalopods diversify their proteomes extensively by RNA editing
•Extensive recoding is specific to the behaviorally complex coleiods
•Unlike mammals, cephalopod recoding is evolutionarily conserved and often adaptive
•Transcriptome diversification comes at the expense of slowed-down genome evolution
RNA editing, a post-transcriptional process, allows the diversification of proteomes beyond the genomic blueprint; however it is infrequently used among animals for this purpose. Recent reports suggesting increased levels of RNA editing in squids thus raise the question of the nature and effects of these events. We here show that RNA editing is particularly common in behaviorally sophisticated coleoid cephalopods, with tens of thousands of evolutionarily conserved sites. Editing is enriched in the nervous system, affecting molecules pertinent for excitability and neuronal morphology. The genomic sequence flanking editing sites is highly conserved, suggesting that the process confers a selective advantage. Due to the large number of sites, the surrounding conservation greatly reduces the number of mutations and genomic polymorphisms in protein-coding regions. This trade-off between genome evolution and transcriptome plasticity highlights the importance of RNA recoding as a strategy for diversifying proteins, particularly those associated with neural function.
coupling between distant biofilms and emergence of nutrient time-sharing
liu j et al. 2017
indolepropionic acid and novel lipid metabolites are associated with a lower risk of type 2 diabetes in the finnish diabetes prevention study
vanessa d. de mello et al. 2017
age-associated microbial dysbiosis promotes intestinal permeability, systemic inflammation, and macrophage dysfunction
netusha thevaranjan et al. 2017
•Age-associated inflammation drives macrophage dysfunction and tissue damage
•Mice under germ-free conditions are protected from age-associated inflammation
•Co-housing germ-free mice with old, but not young, mice increases age-related inflammation
•Age-related microbiota changes can be reversed by reducing TNF levels
Levels of inflammatory mediators in circulation are known to increase with age, but the underlying cause of this age-associated inflammation is debated. We find that, when maintained under germ-free conditions, mice do not display an age-related increase in circulating pro-inflammatory cytokine levels. A higher proportion of germ-free mice live to 600 days than their conventional counterparts, and macrophages derived from aged germ-free mice maintain anti-microbial activity. Co-housing germ-free mice with old, but not young, conventionally raised mice increases pro-inflammatory cytokines in the blood. In tumor necrosis factor (TNF)-deficient mice, which are protected from age-associated inflammation, age-related microbiota changes are not observed. Furthermore, age-associated microbiota changes can be reversed by reducing TNF using anti-TNF therapy. These data suggest that aging-associated microbiota promote inflammation and that reversing these age-related microbiota changes represents a potential strategy for reducing age-associated inflammation and the accompanying morbidity.
differences in gut microbial composition correlate with regional brain volumes in irritable bowel syndrome
jennifer s. labus et al. 2017
legacy effects of developmental stages determine the functional role of predators
volker h. w. rudolf & b. g. van allen 2017
self-motion evokes precise spike timing in the primate vestibular system
mohsen jamali, maurice j. chacron, kathleen e. cullen 2016
fishing down nutrients on coral reefs
jacob e. allgeier, abel valdivia, courtney cox, craig a. layman 2016
what does it mean to be human?
gaia vince discovers that analysing the genetics of ancient humans means changing ideas about our evolution 2017
The things that we thought we understood about Europeans are coming unstuck as we examine the genes of more ancient people. For example, it was generally accepted that pale skin evolved so we could get more vitamin D after moving north to where there was little sun and people had to cover up against the cold. But it turns out that it was the Yamnaya people from much further south, tall and brown-eyed, who brought pale skins to Europe. Northern Europeans before then were dark-skinned and got plenty of vitamin D from eating fish.
It is the same with lactose tolerance. Around 90 per cent of Europeans have a genetic mutation that allows them to digest milk into adulthood, and scientists had assumed that this gene evolved in farmers in northern Europe, giving them an additional food supply to help survive the long winters. But Eske’s research using the genomes of hundreds of Bronze Age people, who lived after the advent of farming, has cast doubt on this theory too: “We found that the genetic trait was almost non-existent in the European population. This trait only became abundant in the northern European population within the last 2,000 years,” he says.
It turns out that lactose tolerance genes were also introduced by the Yamnaya. “They had a slightly higher tolerance to milk than the European farmers and must have introduced it to the European gene pool. Maybe there was a disaster around 2,000 years ago that caused a population bottleneck and allowed the gene to take off. The Viking sagas talk about the sun becoming black – a major volcanic eruption – that could have caused a massive drop in population size, which could have been where some of that stock takes off with lactose.”
ancient human genomes suggest three ancestral populations for present–day humans
neanderthal behaviour, diet, and disease inferred from ancient dna in dental calculus
laura s. weyrich et al. 2017
variable habitat conditions drive species covariation in the human microbiota
charles k. fisher, thierry mora, aleksandra m. walczak 2017
Two species with similar resource requirements respond in a characteristic way to variations in their habitat—their abundances rise and fall in concert. We use this idea to learn how bacterial populations in the microbiota respond to habitat conditions that vary from person-to-person across the human population. Our mathematical framework shows that habitat fluctuations are sufficient for explaining intra-bodysite correlations in relative species abundances from the Human Microbiome Project. We explicitly show that the relative abundances of closely related species are positively correlated and can be predicted from taxonomic relationships. We identify a small set of functional pathways related to metabolism and maintenance of the cell wall that form the basis of a common resource sharing niche space of the human microbiota.
The human body is inhabited by a vast number of microorganisms comprising the human microbiota. The species composition of the microbiota varies considerably from person-to-person and the relative abundances of some species rise and fall in concert. We introduce a mathematical model where differences in habitat conditions cause most of the variability of the microbiota. A statistical analysis shows that variable habitat conditions are sufficient for explaining the patterns of variation observed across a healthy human population and, as a result, the correlation between the relative abundances of two species reflects how closely related they are rather than how they directly interact with each other.
antibiotic-producing symbionts dynamically transition between plant pathogenicity and insect-defensive mutualism
laura v. flórez et al. 2017
endothelial tlr4 and the microbiome drive cerebral cavernous malformations
alan t. tang et al. 2017
sexual dimorphism and retinal mosaic diversification following the evolution of a violet receptor in butterflies
kyle j. mcculloch et al. 2017
microbial genetic composition tunes host longevity
bing han et al. 2017
•Systematic analysis of longevity-promoting microbial genetic variations •Colanic acid as a pro-longevity natural compound effective in different species •Bacterial metabolites regulate host mitochondrial dynamics and UPRmit
Homeostasis of the gut microbiota critically influences host health and aging. Developing genetically engineered probiotics holds great promise as a new therapeutic paradigm to promote healthy aging. Here, through screening 3,983 Escherichia coli mutants, we discovered that 29 bacterial genes, when deleted, increase longevity in the host Caenorhabditis elegans. A dozen of these bacterial mutants also protect the host from age-related progression of tumor growth and amyloid-beta accumulation. Mechanistically, we discovered that five bacterial mutants promote longevity through increased secretion of the polysaccharide colanic acid (CA), which regulates mitochondrial dynamics and unfolded protein response (UPRmt) in the host. Purified CA polymers are sufficient to promote longevity via ATFS-1, the host UPRmt-responsive transcription factor. Furthermore, the mitochondrial changes and longevity effects induced by CA are conserved across different species. Together, our results identified molecular targets for developing pro-longevity microbes and a bacterial metabolite acting on host mitochondria to promote longevity.
"These findings are also interesting and have implications from the biological point of view in the way we understand host-microbe communication," Wang said. "Mitochondria seem to have evolved from bacteria that millions of years ago entered primitive cells. Our finding suggests that products from bacteria today can still chime in the communication between mitochondria in our cells. We think that this type of communication is very important and here we have provided the first evidence of this. Fully understanding microbe-mitochondria communication can help us understand at a deeper level the interactions between microbes and their hosts."
animals in a bacterial world, a new imperative for the life sciences
mcfall–ngai et al 2013
i, superorganism: learning to love your inner ecosystem
jon turney 2015
i contain multitudes: the microbes within us and a grander view of life
ed jong 2016
brain maker: the power of gut microbes to heal and protect your brain — for life
david perlmutter 2015
the gut microbiota of rural papua new guineans: composition, diversity patterns, and ecological processes
inés martínez et al. 2015
•The fecal microbiota in PNG is more diverse but less individualized than in the US
•Most bacterial species are shared among PNG and the US, but abundance profiles differ
•Impact of lifestyle on ecological assembly processes might explain these patterns
•Westernization may decrease bacterial dispersal rates, altering microbiota structure
Although recent research revealed an impact of westernization on diversity and composition of the human gut microbiota, the exact consequences on metacommunity characteristics are insufficiently understood, and the underlying ecological mechanisms have not been elucidated. Here, we have compared the fecal microbiota of adults from two non-industrialized regions in Papua New Guinea (PNG) with that of United States (US) residents. Papua New Guineans harbor communities with greater bacterial diversity, lower inter-individual variation, vastly different abundance profiles, and bacterial lineages undetectable in US residents. A quantification of the ecological processes that govern community assembly identified bacterial dispersal as the dominant process that shapes the microbiome in PNG but not in the US. These findings suggest that the microbiome alterations detected in industrialized societies might arise from modern lifestyle factors limiting bacterial dispersal, which has implications for human health and the development of strategies aimed to redress the impact of westernization.
stochastic assembly produces heterogeneous communities in the caenorhabditis elegans intestine
nicole m. vega, jeff gore 2017
Host-associated bacterial communities vary extensively between individuals, but it can be very difficult to determine the sources of this heterogeneity. Here, we demonstrate that stochastic bacterial community assembly in the Caenorhabditis elegans intestine is sufficient to produce strong interworm heterogeneity in community composition. When worms are fed with two neutrally competing, fluorescently labeled bacterial strains, we observe stochastically driven bimodality in community composition, in which approximately half of the worms are dominated by each bacterial strain. A simple model incorporating stochastic colonization suggests that heterogeneity between worms is driven by the low rate at which bacteria successfully establish new intestinal colonies. We can increase this rate experimentally by feeding worms at high bacterial density; in these conditions, the bimodality disappears. These results demonstrate that demographic noise is a potentially important driver of diversity in bacterial community formation and suggest a role for C. elegans as a model system for ecology of host-associated communities.
Host-associated bacterial communities—also known as microbiomes—vary extensively between individuals, even among clones exposed to the same environment. The sources of this variation are not entirely understood and can be very difficult to determine. In this manuscript, we demonstrate experimentally how randomness in bacterial colonization can result in large differences in the composition of host-associated bacterial communities, using the nematode worm Caenorhabditis elegans as a tractable host model. We find that the amount of variation between individual communities is a function of two rates relevant to how bacteria colonize the host intestine: the colonization rate and the birth rate. We can manipulate the degree of variation between communities by altering the colonization rate, using the amount of bacteria presented to the worms to control the rate at which migrants enter the intestine. When worms are fed with two neutrally competing, fluorescently labeled bacterial strains at low colonization rates, we are able to produce noise-induced bistability in this system, in which each community is dominated by bacteria of only one color. These results demonstrate the potential importance of noise and randomness as a driver of variation between communities and highlight the utility of the simple model organism C. elegans for studying questions relevant to host-associated microbial communities.
system that is stable without diffusion becomes unstable in the presence of diffusion. Turing was motivated to understand morphogenesis with this example of instability
complex pectin metabolism by gut bacteria reveals novel catalytic functions
didier ndeh et al. 2017
exposure to bacterial cpg dna protects from airway allergic inflammation by expanding regulatory lung interstitial macrophages
catherine sabatel et al. 2017
microbes can help explain the evolution of host altruism
ohad lewin-epstein, ranit aharonov & lilach hadany 2017
A new study finds that a noninvasive electromagnetic brain stimulation technique helps obese people lose weight, partly by changing the composition of their intestinal bacteria -- the so-called gut microbiota. Results of the technique, called deep transcranial magnetic stimulation (dTMS), will be presented Sunday at ENDO 2017, the Endocrine Society's 99th annual meeting in Orlando, Fla.
the gut microbiota and autism spectrum disorders
qinrui li, ying han, angel belle c. dy, randi j. hagerman 2017
influencing organism directly
missing microbes: how the overuse of antibiotics is fuelling our modern plagues
martin blaser 2014
psychobiotics and the manipulation of bacteria-brain signals
sarkar et al. 2016
gut microbiota orchestrates energy homeostasis during cold
chevalier et al 2015
the airway microbiome at birth
charitharth vivek lal et al 2016
staphylococcus aureus shifts toward commensalism in response to corynebacterium species
matthew m. ramsey, marcelo o. freire, rebecca a. gabrilska, kendra p. rumbaugh and katherine p. lemon 2016
extreme dysbiosis of the microbiome in critical illness
daniel mcdonald et al 2016
long-term effects on luminal and mucosal microbiota and commonly acquired taxa in faecal microbiota transplantation for recurrent clostridium difficile infection
jonna jalanka et al. 2016
Faecal microbiota transplantation (FMT) is an effective treatment for recurrent Clostridium difficile infection (rCDI). It restores the disrupted intestinal microbiota and subsequently suppresses C. difficile. The long-term stability of the intestinal microbiota and the recovery of mucosal microbiota, both of which have not been previously studied, are assessed herein. Further, the specific bacteria behind the treatment efficacy are also investigated.
We performed a high-throughput microbiota profiling using a phylogenetic microarray analysis of 131 faecal and mucosal samples from 14 rCDI patients pre- and post-FMT during a 1-year follow-up and 23 samples from the three universal donors over the same period.
The FMT treatment was successful in all patients. FMT reverted the patients’ bacterial community to become dominated by Clostridium clusters IV and XIVa, the major anaerobic bacterial groups of the healthy gut. In the mucosa, the amount of facultative anaerobes decreased, whereas Bacteroidetes increased. Post-FMT, the patients’ microbiota profiles were more similar to their own donors than what is generally observed for unrelated subjects and this striking similarity was retained throughout the 1-year follow-up. Furthermore, the universal donor approach allowed us to identify bacteria commonly established in all CDI patients and revealed a commonly acquired core microbiota consisting of 24 bacterial taxa.
FMT induces profound microbiota changes, therefore explaining the high clinical efficacy for rCDI. The identification of commonly acquired bacteria could lead to effective bacteriotherapeutic formulations. FMT can affect microbiota in the long-term and offers a means to modify it relatively permanently for the treatment of microbiota-associated diseases.
dietary zinc alters the microbiota and decreases resistance to clostridium difficile infection
joseph p zackular et al. 2016
gut microbiota and glucometabolic alterations in response to recurrent partial sleep deprivation in normal-weight young individuals
christian benedict, heike vogel, wenke jonas, anni woting, michael blaut, annette schürmann, jonathan cedernaes 2016
prenatal exposure to a mother’s stress contributes to anxiety and cognitive problems that persist into adulthood, a phenomenon that could be explained by lasting – and potentially damaging – changes in the microbiome, according to new research in mice
akkermansia muciniphila mediates negative effects of ifnγ on glucose metabolism
renee l. greer 2016
diet-microbiota interactions mediate global epigenetic programming in multiple host tissues
kimberly a. krautkramer et al. 2016
Gut microbiota alter host histone acetylation and methylation in multiple tissues
Western diet suppresses microbiota-driven SCFA production and chromatin effects
SCFAs recapitulate microbiota-driven chromatin and transcriptional effects
Histone-modifying enzymes regulate transcription and are sensitive to availability of endogenous small-molecule metabolites, allowing chromatin to respond to changes in environment. The gut microbiota produces a myriad of metabolites that affect host physiology and susceptibility to disease; however, the underlying molecular events remain largely unknown. Here we demonstrate that microbial colonization regulates global histone acetylation and methylation in multiple host tissues in a diet-dependent manner: consumption of a “Western-type” diet prevents many of the microbiota-dependent chromatin changes that occur in a polysaccharide-rich diet. Finally, we demonstrate that supplementation of germ-free mice with short-chain fatty acids, major products of gut bacterial fermentation, is sufficient to recapitulate chromatin modification states and transcriptional responses associated with colonization. These findings have profound implications for understanding the complex functional interactions between diet, gut microbiota, and host health.
gut microbiota regulate motor deficits and neuroinflammation in a model of parkinson’s disease
timothy r. sampson et al. 2016
Gut microbes promote α-synuclein-mediated motor deficits and brain pathology
Depletion of gut bacteria reduces microglia activation
SCFAs modulate microglia and enhance PD pathophysiology
Human gut microbiota from PD patients induce enhanced motor dysfunction in mice
The intestinal microbiota influence neurodevelopment, modulate behavior, and contribute to neurological disorders. However, a functional link between gut bacteria and neurodegenerative diseases remains unexplored. Synucleinopathies are characterized by aggregation of the protein α-synuclein (αSyn), often resulting in motor dysfunction as exemplified by Parkinson’s disease (PD). Using mice that overexpress αSyn, we report herein that gut microbiota are required for motor deficits, microglia activation, and αSyn pathology. Antibiotic treatment ameliorates, while microbial re-colonization promotes, pathophysiology in adult animals, suggesting that postnatal signaling between the gut and the brain modulates disease. Indeed, oral administration of specific microbial metabolites to germ-free mice promotes neuroinflammation and motor symptoms. Remarkably, colonization of αSyn-overexpressing mice with microbiota from PD-affected patients enhances physical impairments compared to microbiota transplants from healthy human donors. These findings reveal that gut bacteria regulate movement disorders in mice and suggest that alterations in the human microbiome represent a risk factor for PD.
glyphosate’s suppression of cytochrome p450 enzymes and amino acid biosynthesis by the gut microbiome: pathways to modern diseases
anthony samsel and stephanie seneff 2013
intestinal serotonin transporter inhibition by toll-like receptor 2 activation. a feedback modulation
latorre e, layunta e, grasa l, castro m, pardo j, gomollón f, et al. 2016
the active component of aspirin, salicylic acid, promotes staphylococcus aureus biofilm formation in a pia-dependent manner
cristian dotto et al. 2017
reduction of abeta amyloid pathology in appps1 transgenic mice in the absence of gut microbiota
t. harach et al. 2017
cutaneous leishmaniasis induces a transmissible dysbiotic skin microbiota that promotes skin inflammation
ciara gimblet et al. 2017
Leishmania infection alters the skin microbiota of both humans and mice
Dysbiosis is characterized by a dominance of Staphylococcus and/or Streptococcus
Naive mice acquire dysbiosis when co-housed with leishmania-infected mice
Acquiring a dysbiotic microbiota prior to infection exacerbates skin inflammation
Skin microbiota can impact allergic and autoimmune responses, wound healing, and anti-microbial defense. We investigated the role of skin microbiota in cutaneous leishmaniasis and found that human patients infected with Leishmania braziliensis develop dysbiotic skin microbiota, characterized by increases in the abundance of Staphylococcus and/or Streptococcus. Mice infected with L. major exhibit similar changes depending upon disease severity. Importantly, this dysbiosis is not limited to the lesion site, but is transmissible to normal skin distant from the infection site and to skin from co-housed naive mice. This observation allowed us to test whether a pre-existing dysbiotic skin microbiota influences disease, and we found that challenging dysbiotic naive mice with L. major or testing for contact hypersensitivity results in exacerbated skin inflammatory responses. These findings demonstrate that a dysbiotic skin microbiota is not only a consequence of tissue stress, but also enhances inflammation, which has implications for many inflammatory cutaneous diseases.
influencing bacteriome as well as entire organism directly
drosophila adaptation to viral infection through defensive symbiont evolution
vitor g. faria, nelson e. martins, sara magalhães, tânia f. paulo, viola nolte, christian schlötterer, élio sucena, luis teixeira 2016
Microbial symbionts can modulate host interactions with biotic and abiotic factors. Such interactions may affect the evolutionary trajectories of both host and symbiont. Wolbachia protects Drosophila melanogaster against several viral infections and the strength of the protection varies between variants of this endosymbiont. Since Wolbachia is maternally transmitted, its fitness depends on the fitness of its host. Therefore, Wolbachia populations may be under selection when Drosophila is subjected to viral infection. Here we show that in D. melanogaster populations selected for increased survival upon infection with Drosophila C virus there is a strong selection coefficient for specific Wolbachia variants, leading to their fixation. Flies carrying these selected Wolbachia variants have higher survival and fertility upon viral infection when compared to flies with the other variants. These findings demonstrate how the interaction of a host with pathogens shapes the genetic composition of symbiont populations. Furthermore, host adaptation can result from the evolution of its symbionts, with host and symbiont functioning as a single evolutionary unit.
Animals live in close association with microbial partners that can shape many aspects of their lives. For instance, several insects carry bacteria that defend them against parasites and infectious diseases. The intracellular bacterium Wolbachia protects the fruit fly Drosophila melanogaster against viral infection. Natural populations of Drosophila carry different variants of Wolbachia, which differ from one another in the strength of this protection. Here we show that a population of Drosophila infected with viruses during several generations adapts to this challenge through turnover in Wolbachia composition. The Wolbachia variants that give higher protection to viruses, by increasing fly survival and fecundity upon infection, are strongly selected. This work demonstrates that the interaction of an animal with a pathogen can shape its associated microbial populations. We show that adaptation to pathogens can be achieved not only through selection of resistance on the host proper but also through the evolutionary shaping of its microbial community.
predators catalyze an increase in chloroviruses by foraging on the symbiotic hosts of zoochlorellae
john p. delong, zeina al-ameeli, garry duncan, james l. van etten, david d. dunigan 2016
Reproduction and growth of viruses depend on successful encounters with appropriate hosts. However, some hosts are difficult to encounter. In particular, chloroviruses cannot reach their target zoochlorellae hosts, because zoochlorellae are endosymbionts, living inside the cell of a protist that protects the zoochlorellae from the chlorovirus. The protist host is subject to predation, and we show that copepods foraging on zoochlorellae-bearing protists can disrupt the mutualism and pass endosymbiontic zoochlorellae through their guts, exposing them to chloroviruses. In this way, predators can catalyze the virus population growth by breaking down physical barriers between viruses and their endosymbiont hosts.
Virus population growth depends on contacts between viruses and their hosts. It is often unclear how sufficient contacts are made between viruses and their specific hosts to generate spikes in viral abundance. Here, we show that copepods, acting as predators, can bring aquatic viruses and their algal hosts into contact. Specifically, predation of the protist Paramecium bursaria by copepods resulted in a >100-fold increase in the number of chloroviruses in 1 d. Copepod predation can be seen as an ecological “catalyst” by increasing contacts between chloroviruses and their hosts, zoochlorellae (endosymbiotic algae that live within paramecia), thereby facilitating viral population growth. When feeding, copepods passed P. bursaria through their digestive tract only partially digested, releasing endosymbiotic algae that still supported viral reproduction and resulting in a virus population spike. A simple predator–prey model parameterized for copepods consuming protists generates cycle periods for viruses consistent with those observed in natural ponds. Food webs are replete with similar symbiotic organisms, and we suspect the predator catalyst mechanism is capable of generating blooms for other endosymbiont-targeting viruses.
trim28 controls a gene regulatory network based on endogenous retroviruses in human neural progenitor cells
per ludvik brattås et al. 2017
•Stage- and region-specific expression of ERVs during human brain development
•TRIM28 binds to ERVs and induces hetereochromatin in human neural progenitor cells
•Knockdown of TRIM28 in hNPCs results in the upregulation of ERV expression
•Protein-coding genes located near upregulated ERVs are upregulated
Endogenous retroviruses (ERVs), which make up 8% of the human genome, have been proposed to participate in the control of gene regulatory networks. In this study, we find a region- and developmental stage-specific expression pattern of ERVs in the developing human brain, which is linked to a transcriptional network based on ERVs. We demonstrate that almost 10,000, primarily primate-specific, ERVs act as docking platforms for the co-repressor protein TRIM28 in human neural progenitor cells, which results in the establishment of local heterochromatin. Thereby, TRIM28 represses ERVs and consequently regulates the expression of neighboring genes. These results uncover a gene regulatory network based on ERVs that participates in control of gene expression of protein-coding transcripts important for brain development.
harbouring public good mutants within a pathogen population can increase both fitness and virulence
richard j lindsay et al 2016
human age and skin physiology shape diversity and abundance of archaea on skin
christine moissl-eichinger et al. 2017
Reference: Biol. Bull. 227: 300–312. (December 2014)
FISH Labeling Reveals a Horizontally Transferred Algal (Vaucheria litorea) Nuclear Gene on a Sea Slug (Elysia chlorotica) Chromosome
JULIE A. SCHWARTZ1, NICHOLAS E. CURTIS2, AND SIDNEY K. PIERCE1,3*
1Department of Integrative Biology, University of South Florida, Tampa, Florida 33620; 2Department of Biology and Chemistry, Ave Maria University, Ave Maria, Florida 34142; and 3Department of Biology, University of Maryland, College Park, Maryland 20742
horizontal gene transfer
not only in simple organisms
horizontal gene transfer is more frequent with increased heterotrophy and contributes to parasite adaptation
zhenzhen yang et al. 2016
Horizontal gene transfer (HGT) is the nonsexual transfer and genomic integration of genetic materials between organisms. In eukaryotes, HGT appears rare, but parasitic plants may be exceptions, as haustorial feeding connections between parasites and their hosts provide intimate cellular contacts that could facilitate DNA transfer between unrelated species. Through analysis of genome-scale data, we identified >50 expressed and likely functional HGT events in one family of parasitic plants. HGT reflected parasite preferences for different host plants and was much more frequent in plants with increasing parasitic dependency. HGT was strongly biased toward expression and protein types likely to contribute to haustorial function, suggesting that functional HGT of host genes may play an important role in adaptive evolution of parasites.
Horizontal gene transfer (HGT) is the transfer of genetic material across species boundaries and has been a driving force in prokaryotic evolution. HGT involving eukaryotes appears to be much less frequent, and the functional implications of HGT in eukaryotes are poorly understood. We test the hypothesis that parasitic plants, because of their intimate feeding contacts with host plant tissues, are especially prone to horizontal gene acquisition. We sought evidence of HGTs in transcriptomes of three parasitic members of Orobanchaceae, a plant family containing species spanning the full spectrum of parasitic capabilities, plus the free-living Lindenbergia. Following initial phylogenetic detection and an extensive validation procedure, 52 high-confidence horizontal transfer events were detected, often from lineages of known host plants and with an increasing number of HGT events in species with the greatest parasitic dependence. Analyses of intron sequences in putative donor and recipient lineages provide evidence for integration of genomic fragments far more often than retro-processed RNA sequences. Purifying selection predominates in functionally transferred sequences, with a small fraction of adaptively evolving sites. HGT-acquired genes are preferentially expressed in the haustorium—the organ of parasitic plants—and are strongly biased in predicted gene functions, suggesting that expression products of horizontally acquired genes are contributing to the unique adaptive feeding structure of parasitic plants.
cancer tumors as metazoa 1.0: tapping genes of ancient ancestors
p c w davies and c h lineweaver 2011
canine transmissible venereal tumour
cancer cells enter dormancy after cannibalizing mesenchymal stem/stromal cells (mscs)
thomas j. bartosh, mujib ullah, suzanne zeitouni, joshua beaver, darwin j. prockop 2016
shaping variation in the human immune system
liston, linterman, and carr 2016
Immune responses demonstrate a high level of intra-species variation, compensating for the specialization capacity of pathogens. The recent advent of in-depth immune phenotyping projects in large-scale cohorts has allowed a first look into the factors that shape the inter-individual diversity of the human immune system. Genetic approaches have identified genetic diversity as drivers of 20–40% of the variation between the immune systems of individuals. The remaining 60–80% is shaped by intrinsic factors, with age being the predominant factor, as well as by environmental influences, where cohabitation and chronic viral infections were identified as key mediators. We review and integrate the recent in-depth large-scale studies on human immune diversity and its potential impact on health.
Diversity within the human immune system is stable over the duration of months to years with an elastic response to immunological challenge, allowing the study of immune drivers.
Genetic variation accounts for 20–40% of immune variation, with enrichment of gene variants associated with autoimmunity, inflammatory disease, and susceptibility to infections among the identified genetic drivers.
Among the identified intrinsic drivers of immune variation, age is the most potent, driving a shift from a precursor-biased immune status to an inflammation-biased immune status.
A strong environmental effect on immune variation is observed, as revealed by cohabitation studies, with the strongest individual driver identified to date being chronic viral infection.
bacterial immune system
quorum sensing controls adaptive immunity through the regulation of multiple crispr-cas systems
adrian g. patterson et al. 2016
Quorum sensing regulates the type I-E, I-F, and III-A CRISPR-Cas systems in Serratia
SmaR represses cas gene and CRISPR expression in the absence of AHL signals
Both interference and adaptation are modulated by quorum sensing
Bacteria coordinate their defenses based on cell density and the risk of infection
Bacteria commonly exist in high cell density populations, making them prone to viral predation and horizontal gene transfer (HGT) through transformation and conjugation. To combat these invaders, bacteria possess an arsenal of defenses, such as CRISPR-Cas adaptive immunity. Many bacterial populations coordinate their behavior as cell density increases, using quorum sensing (QS) signaling. In this study, we demonstrate that QS regulation results in increased expression of the type I-E, I-F, and III-A CRISPR-Cas systems in Serratia cells in high-density populations. Strains unable to communicate via QS were less effective at defending against invaders targeted by any of the three CRISPR-Cas systems. Additionally, the acquisition of immunity by the type I-E and I-F systems was impaired in the absence of QS signaling. We propose that bacteria can use chemical communication to modulate the balance between community-level defense requirements in high cell density populations and host fitness costs of basal CRISPR-Cas activity.
immune system where we didn’t expect it
structural and functional features of central nervous system lymphatic vessels
antoine louveau et al. 2015
egress of sperm autoantigen from seminiferous tubules maintains systemic tolerance
kenneth s.k. tung et al. 2017
evolution through loss is different from evolution through gain. currently evolution through gain.
genetic basis for race
nicholas wade 2014 a troublesome inheritance: genes, race, and human history
the 10,000 year explosion; how civilization accelerated human evolution
gregory cochran, henry harpending 2009
cultural basis for healthy habits
dna dispose, but subjects decide. learning and the extended synthesis
markus lindholm 2015
living space, not competition, is evolutionary driver?
this is particularly important because "evolutionary competition" "nature red in tooth and claw" is a prime assumption of our society.
links between global taxonomic diversity, ecological diversity and the expansion of vertebrates on land
sahney et al 2010
evolutionary rescue can prevent extinction following environmental change
graham bell and andrew gonzalez 2009
basically, presence of a few adapted individuals in a large population allows numbers to recover in laboratory i.e. stable conditions. changing conditions not investigated here, only single step change.
The ubiquity of global change and its impacts on biodiversity poses a clear and urgent challenge for evolutionary biologists. In many cases, environmental change is so widespread and rapid that individuals can neither accommodate to them physiologically nor migrate to a more favourable site. Extinction will ensue unless the population adapts fast enough to counter the rate of decline. According to theory, whether populations can be rescued by evolution depends upon several crucial variables: population size, the supply of genetic variation, and the degree of maladaptation to the new environment. Using techniques in experimental evolution we tested the conditions for evolutionary rescue (ER). Hundreds of yeast populations were exposed to normally lethal concentrations of salt in conditions, where the frequency of rescue mutations was estimated and population size was manipulated. In a striking match with theory, we show that ER is possible, and that the recovery of the population may occur within 25 generations. We observed a clear threshold in population size for ER whereby the ancestral population size must be sufficiently large to counter stochastic extinction and contain resistant individuals. These results demonstrate that rapid evolution is an important component of the response of small populations to environmental change.
interface theory of perception http://www.cogsci.uci.edu/~ddhoff/interface.pdf
is our next evolutionary step to learn to control these massive ponderous structures that we have built, of industry, of law, of everything? we are still operating as a society on the individual level and have poor control over the direction of our society.
“junk” dna is not junk
genomic variation within alpha satellite dna influences centromere location on human chromosomes with metastable epialleles
megan e aldrup-macdonald, molly e kuo, lori l sullivan, kimberline chew, beth a sullivan 2016;
l1-associated genomic regions are deleted in somatic cells of the healthy human brain
jennifer erwin et al. 2016
occurrence of harmful gene variants could be the price we pay for the genetic diversity that is otherwise highly beneficial to our survival
excess of deleterious mutations around hla genes reveals evolutionary cost of balancing selection
tobias l. lenz, victor spirin, daniel m. jordan, shamil r. sunyaev 2016
social context, but not individual personality, alters immigrant viability in a spider with mixed social structure
spencer j. ingley, jonathan n. pruitt, inon scharf, jessica purcell 2016
demographic and reproductive plasticity across the depth distribution of a coral reef fish
esther d. goldstein, evan k. d’alessandro, su sponaugle 2016
archean coastal-plain paleosols and life on land
gregory j. retallack, david h. krinsley, robert fischer, joshua j. razink, kurt a. langworthy 2016
There are coastal-plain paleosols in 3.0 Ga Farrel Quartzite, Western Australia.
Paleosols have organic surface (A) and sulfate-rich subsurface (By) horizon.
Comparable profiles are known from deserts of Chile, Antarctica, and Mars.
Microfossils in paleosols include actinobacteria, sulfur bacteria, methanogens.
Coastal-plain paleosols in the 3.0 Ga Farrel Quartzite of Western Australia have organic surface (A horizon) and sulfate-rich subsurface (By) horizons, like soils of the Atacama Desert of Chile, Dry Valleys of Antarctica, and 3.7 Ga paleosols of Mars. Farrel Quartzite paleosols include previously described microfossils, permineralized by silica in a way comparable with the Devonian Rhynie Chert, a well known permineralized Histosol. Five microfossil morphotypes in the Farrel Quartzite include a variety of spheroidal cells (Archaeosphaeroides) as well as distinctive large spindles (new genus provisionally assigned to cf. Eopoikilofusa). Previously published cell-specific carbon isotopic analyses of the Farrel Quartzite microfossils, and unusually abundant sulfate considering a likely anoxic atmosphere, allow interpretation of these morphotypes as a terrestrial community of actinobacteria, purple sulfur bacteria, and methanogenic Archaea.
the 'out of africa' hypothesis, human genetic diversity, and comparative economic development
quamrul ashraf, oded galor 2013
mutations and sexual recombination transmitted via DNA, distribution changes and also elimination via genetic drift and migration
defined chromosome structure in the genome-reduced bacterium mycoplasma pneumoniae
marie trussart et al. 2017
evolutionary development biology
methylation during lifetime transmitted via germline
maternal h3k27me3 controls dna methylation-independent imprinting
azusa inoue, lan jiang, falong lu, tsukasa suzuki, yi zhang 2017
parent-of-origin dna methylation dynamics during mouse development
yonatan stelzer, hao wu, yuelin song, chikdu s. shivalila, styliani markoulaki, rudolf jaenisch 2016
•In vivo tracing of parent-specific DNA methylation dynamics at single-cell resolution
•Cell-type-specific methylation signatures at the Dlk-Dio3 IG-DMR during development
•Dynamic parent- and cell-type-specific DNA methylation changes in the adult brain
Parent-specific differentially methylated regions (DMRs) are established during gametogenesis and regulate parent-specific expression of imprinted genes. Monoallelic expression of imprinted genes is essential for development, suggesting that imprints are faithfully maintained in embryos and adults. To test this hypothesis, we targeted a reporter for genomic methylation to the imprinted Dlk1-Dio3 intergenic DMR (IG-DMR) to assess the methylation of both parental alleles at single-cell resolution. Biallelic gain or loss of IG-DMR methylation occurred in a small fraction of mouse embryonic stem cells, significantly affecting developmental potency. Mice carrying the reporter in either parental allele showed striking parent-specific changes in IG-DMR methylation, causing substantial and consistent tissue- and cell-type-dependent signatures in embryos and postnatal animals. Furthermore, dynamics in DNA methylation persisted during adult neurogenesis, resulting in inter-individual diversity. This substantial cell-cell DNA methylation heterogeneity implies that dynamic DNA methylation variations in the adult may be of functional importance.
krab zinc-finger proteins contribute to the evolution of gene regulatory networks
michaël imbeault, pierre-yves helleboid, didier trono 2017
germ line-inherited h3k27me3 restricts enhancer function during maternal-to-zygotic transition
zenk f et al. 2017
the epitranscriptome of noncoding rnas in cancer
manel esteller, pier paolo pandolfi 2017
reconsidering plant memory: intersections between stress recovery, rna turnover, and epigenetics
crisp et al. 2016
intrinsically disordered proteins drive emergence and inheritance of biological traits
sohini chakrabortee et al. 2016
genetic evidence for elevated pathogenicity of mitochondrial dna heteroplasmy in autism spectrum disorder
wang y, picard m, gu z 2016
classification and adaptive behavior prediction of children with autism spectrum disorder based upon multivariate data analysis of markers of oxidative stress and dna methylation
daniel p. howsmon, uwe kruger, stepan melnyk, s. jill james, juergen hahn 2017
mitochondrial dysfunction in autism spectrum disorders: a systematic review and meta-analysis
d a rossignol, r e frye 2011
mitochondrial function controls intestinal epithelial stemness and proliferation
emanuel berger et al. 2016
perhaps conscious change in particular direction can lead to epigenetic change
they continue to look for pathways in which, for example, serotonin directly influences behavior via chemical changes in the brain. but what if the real mechanism is actually indirect, that epigenetic changes are constantly happening and what serotonin does is tip the balance towards a certain population of epigenetic variance, which in turn causes the behavior we observe
when I get enough sleep, ideas and connections and creativity just seem to flow. could this be through epigenetic change too?
adolescent binge-pattern alcohol exposure alters genome-wide dna methylation patterns in the hypothalamus of alcohol-naïve male offspring
annadorothea animes 2016
cell autonomous regulation of herpes and influenza virus infection by the circadian clock
rachel s. edgara et al. 2016
local modulation of human brain responses by circadian rhythmicity and sleep debt
vincenzo muto et al 2016
microbiota diurnal rhythmicity programs host transcriptome oscillations
christoph a. thaiss et al. 2016
Intestinal microbiota biogeography and metabolome undergo diurnal oscillations
Circadian oscillations of serum metabolites are regulated by the microbiota
Microbiota rhythms program the circadian epigenetic and transcriptional landscape
The microbiota regulates the circadian liver transcriptome and detoxification pattern
The intestinal microbiota undergoes diurnal compositional and functional oscillations that affect metabolic homeostasis, but the mechanisms by which the rhythmic microbiota influences host circadian activity remain elusive. Using integrated multi-omics and imaging approaches, we demonstrate that the gut microbiota features oscillating biogeographical localization and metabolome patterns that determine the rhythmic exposure of the intestinal epithelium to different bacterial species and their metabolites over the course of a day. This diurnal microbial behavior drives, in turn, the global programming of the host circadian transcriptional, epigenetic, and metabolite oscillations. Surprisingly, disruption of homeostatic microbiome rhythmicity not only abrogates normal chromatin and transcriptional oscillations of the host, but also incites genome-wide de novo oscillations in both intestine and liver, thereby impacting diurnal fluctuations of host physiology and disease susceptibility. As such, the rhythmic biogeography and metabolome of the intestinal microbiota regulates the temporal organization and functional outcome of host transcriptional and epigenetic programs.
top of the world
such a feeling’s coming over me
there is wonder in most every thing i see
not a cloud in the sky, got the sun in my eyes
and i won’t be surprised if it’s a dream
everything i want the world to be
is now coming true especially for me
and the reason is clear, it’s because you are here
you’re the nearest thing to heaven that i’ve seen
☆i’m on the top of the world looking down on creation
and the only explanation i can find
is the love that i’ve found ever since you’ve been around
your love’s put me at the top of the world
something in the wind has learned my name
and it’s telling me that things are not the same
in the leaves on the trees and the touch of the breeze
there’s a pleasing sense of happiness for me
there is only one wish on my mind
when this day is through i hope that i will find
that tomorrow will be just the same for you and me
all i need will be mine if you are here