scholarly journals Methylation patterns at fledging predict delayed dispersal in a cooperatively breeding bird

PLoS ONE ◽  
2021 ◽  
Vol 16 (6) ◽  
pp. e0252227
Author(s):  
Andrea L. Liebl ◽  
Jeff S. Wesner ◽  
Andrew F. Russell ◽  
Aaron W. Schrey
Keyword(s):  
First Year ◽  
Breeding Bird ◽  
Delayed Dispersal ◽  
Genome Wide ◽  
A Genome ◽  
Cooperatively Breeding ◽  
Dispersal Behavior ◽  
Natal Habitat ◽  
Indirect Fitness ◽  
Methylation Patterns

Individuals may delay dispersing from their natal habitat, even after maturation to adulthood. Such delays can have broad consequences from determining population structure to allowing an individual to gain indirect fitness by helping parents rear future offspring. Dispersal in species that use delayed dispersal is largely thought to be opportunistic; however, how individuals, particularly inexperienced juveniles, assess their environments to determine the appropriate time to disperse is unknown. One relatively unexplored possibility is that dispersal decisions are the result of epigenetic mechanisms interacting between a genome and environment during development to generate variable dispersive phenotypes. Here, we tested this using epiRADseq to compare genome-wide levels of DNA methylation of blood in cooperatively breeding chestnut-crowned babblers (Pomatostomus ruficeps). We measured dispersive and philopatric individuals at hatching, before fledging, and at 1 year (following when first year dispersal decisions would be made). We found that individuals that dispersed in their first year had a reduced proportion of methylated loci than philopatric individuals before fledging, but not at hatching or as adults. Further, individuals that dispersed in the first year had a greater number of loci change methylation state (i.e. gain or lose) between hatching and fledging. The existence and timing of these changes indicate some influence of development on epigenetic changes that may influence dispersal behavior. However, further work needs to be done to address exactly how developmental environments may be associated with dispersal decisions and which loci in particular are manipulated to generate such changes.

scholarly journals A Genome-Wide Study of DNA Methylation Patterns and Gene Expression Levels in Multiple Human and Chimpanzee Tissues

PLoS Genetics ◽  
2011 ◽  
Vol 7 (2) ◽  
pp. e1001316 ◽  
Author(s):  
Athma A. Pai ◽  
Jordana T. Bell ◽  
John C. Marioni ◽  
Jonathan K. Pritchard ◽  
Yoav Gilad
Keyword(s):  
Gene Expression ◽  
Dna Methylation ◽  
Expression Levels ◽  
Genome Wide ◽  
A Genome ◽  
Methylation Patterns ◽  
Genome Wide Study ◽  
Gene Expression Levels

scholarly journals Kinship affects investment by helpers in a cooperatively breeding bird

2010 ◽  
Vol 277 (1698) ◽  
pp. 3299-3306 ◽  
Author(s):  
Ki-Baek Nam ◽  
Michelle Simeoni ◽  
Stuart P. Sharp ◽  
Ben J. Hatchwell
Keyword(s):  
Cooperative Breeding ◽  
Kin Selection ◽  
Genetic Relatedness ◽  
Critical Role ◽  
Breeding Systems ◽  
Pedigree Information ◽  
Breeding Bird ◽  
Cooperatively Breeding ◽  
Indirect Fitness ◽  
Fitness Benefits

Helping behaviour in cooperative breeding systems has been attributed to kin selection, but the relative roles of direct and indirect fitness benefits in the evolution of such systems remain a matter of debate. In theory, helpers could maximize the indirect fitness benefits of cooperation by investing more in broods with whom they are more closely related, but there is little evidence for such fine-scale adjustment in helper effort among cooperative vertebrates. In this study, we used the unusual cooperative breeding system of the long-tailed tit Aegithalos caudatus to test the hypothesis that the provisioning effort of helpers was positively correlated with their kinship to broods. We first use pedigrees and microsatellite genotypes to characterize the relatedness between helpers and breeders from a 14 year field study. We used both pedigree and genetic approaches because long-tailed tits have access to pedigree information acquired through social relationships, but any fitness consequences will be determined by genetic relatedness. We then show using both pedigrees and genetic relatedness estimates that alloparental investment by helpers increases as their relatedness to the recipients of their care increases. We conclude that kin selection has played a critical role in moulding the investment decisions of helpers in this cooperatively breeding species.

scholarly journals Consequences of ‘load-lightening’ for future indirect fitness gains by helpers in a cooperatively breeding bird

2010 ◽  
Vol 79 (3) ◽  
pp. 529-537 ◽  
Author(s):  
Jessica Meade ◽  
Ki-Baek Nam ◽  
Andrew P. Beckerman ◽  
Ben J. Hatchwell
Keyword(s):  
Breeding Bird ◽  
Cooperatively Breeding ◽  
Indirect Fitness

scholarly journals Complete Metamorphosis in Manduca sexta Involves Specific Changes in DNA Methylation Patterns

2021 ◽  
Vol 9 ◽  
Author(s):  
Jasmin Gegner ◽  
Heiko Vogel ◽  
André Billion ◽  
Frank Förster ◽  
Andreas Vilcinskas
Keyword(s):  
Dna Methylation ◽  
Manduca Sexta ◽  
Histone Deacetylases ◽  
Transcriptional Reprogramming ◽  
Evolution And Development ◽  
Genome Wide ◽  
A Genome ◽  
Genes Encoding ◽  
Methylation Patterns ◽  
Complete Metamorphosis

The transition between morphologically distinct phenotypes during complete metamorphosis in holometabolous insects is accompanied by fundamental transcriptional reprogramming. Using the tobacco hornworm (Manduca sexta), a powerful model for the analysis of insect evolution and development, we conducted a genome-wide comparative analysis of gene expression and DNA methylation in caterpillars and adults to determine whether complete metamorphosis has an epigenetic basis in this species. Bisulfite sequencing indicated a generally low level of DNA methylation with a unimodal CpGO/E distribution. Expression analysis revealed that 24 % of all known M. sexta genes (3.729) were upregulated in last-instar larvae relative to the adult moth, whereas 26 % (4.077) were downregulated. We also identified 4.946 loci and 4.960 regions showing stage-specific differential methylation. Interestingly, genes encoding histone acetyltransferases and histone deacetylases were differentially methylated in the larvae and adults, indicating there is crosstalk between different epigenetic mechanisms. The distinct sets of methylated genes in M. sexta larvae and adults suggest that complete metamorphosis involves epigenetic modifications associated with profound transcriptional reprogramming, involving approximately half of all the genes in this species.

scholarly journals Thorough statistical analyses of breast cancer co-methylation patterns

2021 ◽  
Author(s):  
Shuying Sun ◽  
Jael Dammann ◽  
Pierce Lai ◽  
Christine Tian
Keyword(s):  
Breast Cancer ◽  
Large Datasets ◽  
Chromosome X ◽  
Correlation Pattern ◽  
Network Analyses ◽  
Illumina 450K ◽  
Genome Wide ◽  
A Genome ◽  
Highly Correlated ◽  
Methylation Patterns

Abstract Background Breast cancer is one of the most commonly diagnosed cancers. It is associated with DNA methylation, an epigenetic event with a methyl group added to a cytosine paired with a guanine, i.e., a CG site. The methylation levels of different genes in a genome are correlated in certain ways that affect gene functions. This correlation pattern is known as co-methylation. It is still not clear how different genes co-methylate in the whole genome of breast cancer samples. Previous studies are conducted using relatively small datasets (Illumina 27K data). In this study, we analyze much larger datasets (Illumina 450K data). Results Our key findings are summarized below. First, normal samples have more highly correlated, or co-methylated, CG pairs than tumor samples. Both tumor and normal have more than 93% of positive co-methylation, but normal samples have significantly more negatively correlated CG sites than tumor samples (6.6% vs. 2.8%). Second, both tumor and normal samples have about 94% of co-methylated CG pairs on different chromosomes, but normal samples have 470 million more CG pairs. Highly co-methylated pairs on the same chromosome tend to be close to each other. Third, a small proportion of CG sites’ co-methylation patterns change dramatically from normal to tumor. The percentage of differentially methylated (DM) sites among them is larger than the overall DM rate. Fourth, certain CG sites are highly correlated with many CG sites; the top 100 of such super-connector CG sites in tumor and normal samples have no overlaps. Fifth, both highly changing sites and super-connector sites’ locations are significantly different from the genome-wide CG sites’ locations. Sixth, chromosome X co-methylation patterns are very different from other chromosomes. Finally, the network analyses of genes associated with several sets of co-methylated CG sites identified above show that tumor and normal samples have different patterns. Conclusions Our findings will provide researchers with a new understanding of co-methylation patterns in breast cancer. Our ability to thoroughly analyze co-methylation of large datasets will allow researchers to study relationships and associations between different genes in breast cancer.

scholarly journals Hamilton's inclusive fitness maintains heritable altruism polymorphism through rb = c

2018 ◽  
Vol 115 (8) ◽  
pp. 1860-1864 ◽  
Author(s):  
Changcao Wang ◽  
Xin Lu
Keyword(s):  
Reproductive Success ◽  
Inclusive Fitness ◽  
Lifetime Reproductive Success ◽  
Adult Males ◽  
Breeding Bird ◽  
Annual Fluctuation ◽  
The Social ◽  
Cooperatively Breeding ◽  
Social Partners ◽  
Indirect Fitness

How can altruism evolve or be maintained in a selfish world? Hamilton’s rule shows that the former process will occur when rb > c—the benefits to the recipients of an altruistic act b, weighted by the relatedness between the social partners r, exceed the costs to the altruists c—drives altruistic genotypes spreading against nonaltruistic ones. From this rule, we infer that altruistic genotypes will persist in a population by forming a stable heritable polymorphism with nonaltruistic genotypes if rb = c makes inclusive fitness of the two morphs equal. We test this prediction using the data of 12 years of study on a cooperatively breeding bird, the Tibetan ground tit Pseudopodoces humilis, where helping is performed by males only and kin-directed. Individual variation in ever acting as a helper was heritable (h2 = 0.47), and the resultant altruism polymorphism remained stable as indicated by low-level annual fluctuation of the percentage of helpers among all adult males (24–28%). Helpers’ indirect fitness gains from increased lifetime reproductive success of related breeders statistically fully compensated for their lifetime direct fitness losses, suggesting that rb = c holds. While our work provides a fundamental support for Hamilton’s idea, it highlights the equivalent inclusive fitness returns to altruists and nonaltruists mediated by rb = c as a theoretically and realistically important mechanism to maintain social polymorphism.

scholarly journals Thorough Statistical Analyses of Breast Cancer Co-methylation Patterns

2021 ◽  
Author(s):  
Shuying Sun ◽  
Jael Dammann ◽  
Pierce Lai ◽  
Christine Tian
Keyword(s):  
Breast Cancer ◽  
Large Datasets ◽  
Chromosome X ◽  
Correlation Pattern ◽  
Network Analyses ◽  
Illumina 450K ◽  
Genome Wide ◽  
A Genome ◽  
Highly Correlated ◽  
Methylation Patterns

Abstract Background: Breast cancer is one of the most commonly diagnosed cancers. It is associated with DNA methylation, an epigenetic event with a methyl group added to a cytosine paired with a guanine, i.e., a CG site. The methylation levels of different genes in a genome are correlated in certain ways that affect gene functions. This correlation pattern is known as co-methylation. It is still not clear how different genes co-methylate in the whole genome of breast cancer samples. Previous studies are conducted using relatively small datasets (Illumina 27K data). In this study, we analyze much larger datasets (Illumina 450K data). Results: Our key findings are summarized below. First, normal samples have more highly correlated, or co-methylated, CG pairs than tumor samples. Both tumor and normal have more than 93% of positive co-methylation, but normal samples have significantly more negatively correlated CG sites than tumor samples (6.6% vs. 2.8%). Second, both tumor and normal samples have about 94% of co-methylated CG pairs on different chromosomes, but normal samples have 470 million more CG pairs. Highly co-methylated pairs on the same chromosome tend to be close to each other. Third, a small proportion of CG sites’ co-methylation patterns change dramatically from normal to tumor. The percentage of differentially methylated (DM) sites among them is larger than the overall DM rate. Fourth, certain CG sites are highly correlated with many CG sites; the top 100 of such super-connector CG sites in tumor and normal samples have no overlaps. Fifth, both highly changing sites and super-connector sites’ locations are significantly different from the genome-wide CG sites’ locations. Sixth, chromosome X co-methylation patterns are very different from other chromosomes. Finally, the network analyses of genes associated with several sets of co-methylated CG sites identified above show that tumor and normal samples have different patterns. Conclusions: Our findings will provide researchers with a new understanding of co-methylation patterns in breast cancer. Our ability to thoroughly analyze co-methylation of large datasets will allow researchers to study relationships and associations between different genes in breast cancer.

scholarly journals The fitness consequences of kin-biased dispersal in a cooperatively breeding bird

2015 ◽  
Vol 11 (7) ◽  
pp. 20150336 ◽  
Author(s):  
Lea Pollack ◽  
Dustin R. Rubenstein
Keyword(s):  
Social Rank ◽  
Group Living ◽  
Breeding Bird ◽  
Direct Benefits ◽  
Fitness Consequences ◽  
Cooperatively Breeding ◽  
Potential Benefits ◽  
Indirect Fitness ◽  
Living Species

Cooperative alliances among kin may not only lead to indirect fitness benefits for group-living species, but can also provide direct benefits through access to mates or higher social rank. However, the immigrant sex in most species loses any potential benefits of living with kin unless immigrants disperse together or recruit relatives into the group in subsequent years. To look for evidence of small subgroups of related immigrants within social groups (kin substructure), we used microsatellites to assess relatedness between immigrant females of the cooperatively breeding superb starling, Lamprotornis superbus. We determined how timing of immigration led to kin subgroup formation and if being part of one influenced female fitness. Although mean relatedness in groups was higher for males than females, 26% of immigrant females were part of a kin subgroup with a sister. These immigrant sibships formed through kin recruitment across years more often than through coalitions immigrating together in the same year. Furthermore, females were more likely to breed when part of a kin subgroup than when alone, suggesting that female siblings form alliances that may positively influence their fitness. Ultimately, kin substructure should be considered when determining the role of relatedness in the evolution of animal societies.

Abstract MP31: DNA Methylation Patterns are Associated with Genetic Variation and Systemic Inflammation

Circulation ◽  
2013 ◽  
Vol 127 (suppl_12) ◽  
Author(s):  
Stella Aslibekyan ◽  
Alexis C Frazier-Wood ◽  
Devin M Absher ◽  
Jin Sha ◽  
Degui Zhi ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Systemic Inflammation ◽  
Quantitative Trait ◽  
Inflammatory Marker ◽  
Lipid Lowering ◽  
Chromosome 11 ◽  
Chromosome 20 ◽  
Genome Wide ◽  
A Genome ◽  
Methylation Patterns

Introduction: Chronic systemic inflammation is a complex trait characterized by moderate to high heritability and important implications for cardiovascular health. Previously identified genetic polymorphisms explain only a modest fraction of variability in circulating inflammatory marker concentrations. Hypothesis: We hypothesized that variation in DNA methylation patterns contributes to the missing heritability of inflammatory traits, and that such associations may in turn be influenced by environmental factors (smoking, alcohol, and obesity) as well as common genetic variants. Methods: Using data from the Genetics of Lipid Lowering Drugs and Diet Network (GOLDN, n= 593), we assayed the methylation status of approximately 450,000 sites across the genome and measured serum concentrations of high-sensitivity C-reactive protein (hsCRP), soluble interleukin-2 receptor alpha (sIL2Ra), interleukin-6 (IL6), tumor necrosis factor alpha (TNFa), and monocyte chemoattractant protein 1 (MCP1). To investigate and validate the associations between DNA methylation patterns and systemic inflammation, we split the GOLDN data set into discovery (n= 451) and replication (n= 142) data sets. During the discovery stage, we modeled continuous methylation scores at each site on inflammatory markers, adjusted for age, sex, study site, and T-cell purity as fixed effects and family structure as a random effect. Results: After correcting for multiple comparisons, the strongest signal was obtained from an intergenic CpG island on chromosome 20 and levels of hsCRP (P=5×10-10) and sILR2a (P=6×10-6). Our findings are consistent with previous linkage studies that have identified a quantitative trait locus for inflammation in an adjacent region of chromosome 20. Moreover, the association with sIL2Ra but not hsCRP was observed in replication analyses (P=0.008). Models adjusting for current smoking status, alcohol consumption, or body mass index did not appreciably change the estimates of association. Finally, we performed a genome-wide analysis to identify quantitative trait loci for methylation of the CpG site on chromosome 20. We found a genome-wide significant (P=3×10×-8) association with rs11223480 on chromosome 11 in OPCML, which encodes a tumor suppressor, and suggestive (P<4×10-6) associations with a cluster of 9 variants located on chromosome 20 in MACROD2, a gene previously reported to be associated with systemic inflammation. Conclusions: We have conducted the first integrated study of epigenetic variation, genotype, and circulating inflammatory marker concentrations. In conclusion, our findings suggest that differential methylation of an intergenic region on chromosome 20, likely in conjunction with the underlying genotype, is associated with systemic inflammation and merits further evaluation as a cardiovascular risk factor.

scholarly journals DNA methylation marks inter-nucleosome linker regions throughout the human genome

2013 ◽  
Author(s):  
Benjamin P. Berman ◽  
Yaping Liu ◽  
Theresa K. Kelly
Keyword(s):  
Dna Methylation ◽  
Binding Sites ◽  
Ctcf Binding ◽  
Cpg Dinucleotides ◽  
Nucleosome Organization ◽  
Genome Wide ◽  
A Genome ◽  
Sequencing Studies ◽  
Methylation Patterns

Nucleosome organization and DNA methylation are two epigenetic mechanisms that are important for proper control of mammalian transcription. Numerous lines of evidence suggest an interaction between these two mechanisms, but the nature of this interaction in vivo remains elusive. Whole-genome DNA methylation sequencing studies have shown that human methylation levels are periodic at intervals of approximately 190 bp, suggesting a genome-wide relationship between the two marks. A recent report (Chodavarapu et al., 2010) attributed this to higher methylation levels of DNA within nucleosomes. Here, we propose an alternate explanation for these nucleosomal periodicities. By examining methylation patterns in published datasets, we find that genome-wide methylation levels are highest within the linker regions that occur between nucleosomes in multi-nucleosome arrays. This effect is most prominent within long-range Partially Methylated Domains (PMDs) and the strongly positioned nucleosomes that flank CTCF binding sites. The CTCF-flanking nucleosomes retain positioning even in regions completely devoid of CpG dinucleotides, suggesting that DNA methylation is not required for proper positioning. We propose that DNA methylation is inhibited by histone proteins at CTCF and other unknown classes of nucleosomes within PMDs.

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