mohsen jamali, maurice j. chacron, kathleen e. cullen 2016
sarah j. ivory, margaret w. blome, john w. king, michael m. mcglue, julia e. cole, andrew s. cohen 2016
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.
jacob e. allgeier, abel valdivia, courtney cox, craig a. layman 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
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
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.
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, eero mattila, hanne jouhten, jorn hartman, willem m. de vos, perttu arkkila, reetta satokari 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.
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.
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.
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
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.
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.
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
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.
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
spencer j. ingley, jonathan n. pruitt, inon scharf, jessica purcell 2016
esther d. goldstein, evan k. d’alessandro, su sponaugle 2016
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.
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
evolutionary development biology
methylation during lifetime transmitted via germline
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.
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
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