Search bioRxiv⌕ Search

bioRxiv · 10.1101/139634

Changes Of Gene Expression But Not Cytosine Methylation Are Associated With Behavioural Plasticity Of Parental Care

Abstract

Behaviour is often on the front line of plasticity in response to different environments. At the genetic level, behavioural changes are likely to be associated with changes of gene expression. Most studies to date have focused on gene expression differences associated with discrete behavioural states reflecting development or age-related changes, such as honey bee castes. However, more rapidly flexible behaviour is often observed in response to social context or simple individual variation. The differences in genetic influences for the different forms of plasticity are poorly understood. In this study we contrasted gene expression during male parental care of the burying beetle, Nicrophorus vespilloides, in a factorial design. Male N. vespilloides males typically do not provide care when females are present. However, male care is inducible by the removing female and has parental effects equivalent to female care. We used this experimental manipulation to isolate gene expression and cytosine methylation associated with differences of behavioural state, differences of social context, or differences of individual flexibility for expressing care. The greatest number of differentially expressed genes was associated with behavioural state, followed by differences of social contexts, and lastly differences of individual variation. DNA methylation has been hypothesized to regulate the transcriptional architecture that regulates behavioural transitions. We tested this hypothesis by quantifying differences of cytosine methylation that were associated with differences of behavioural state and individual flexibility. Changes of cytosine methylation were not associated with changes of gene expression. Our results suggest a hierarchical association between gene expression and the different sources of variation that influence behaviour, but that this process is not controlled by DNA methylation despite reflecting levels of plasticity in behaviour. Our results further suggest that the extent that a behaviour is transient plays an underappreciated role in determining the molecular mechanisms that underpin the behaviour.

Source connections

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Cunningham, C. B., Ji, L., McKinney, E. C., Benowitz, K. M., Schmitz, R. J., Moore, A. J.. 2017-05-19. Changes Of Gene Expression But Not Cytosine Methylation Are Associated With Behavioural Plasticity Of Parental Care. https://doi.org/10.1101/139634

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

Mapping, stacking and characterization of a novel resistance haplotype against GpaVvrn-virulent Globodera pallida derived from wild potato relative Solanum brevicaule

Potato production is threatened by pests and pathogens. Among the most harmful are the potato cyst nematodes (PCN), including Globodera pallida. The major control measures are potato cultivars harbouring resistance genes. However, virulent nematode populations are breaking through the most broadly applied resistance genes, and therefore novel resistance genes are required to keep control of G. pallida. In this study we map a resistance locus in wild potato relative Solanum brevicaule to the bottom of chromosome 11 (42.83 - 42.85 Mb) using a k-mer based bulked segregant analysis and name the resistant haplotype GpaXIbrc. The presence of the GpaXIbrc marker in the potato genome significantly increases resistance against a GpaVvrn-virulent G. pallida population (AMPOP01). Furthermore, the GpaXIbrc haplotype was stacked with three other resistance haplotypes: GpaXItar, GpaVvrn, and GpaIXvrn. Stacking of the novel GpaXIbrc haplotype to these other resistance haplotypes resulted in a significant increase in resistance. The largest effect was seen in combinations with 'major' resistance haplotypes GpaVvrn + GpaIXvrn and GpaXItar + GpaXIbrc. To determine whether we are dealing with a novel allele, the resistance mechanism underlying the GpaXIbrc haplotype was described after performing an in vitro bioassay. The resistance mechanism was different from GpaXIspl as described in literature, which is also localized at the bottom of chromosome 11. Therefore, we conclude that we found a novel resistance allele originating from S. brevicaule.

genetics↗

Cellular context shapes the transcriptomic impact of somatic variants

Somatic SNVs are commonly prioritized by recurrence or sequence annotation, leaving the molecular consequences of private variants unresolved. We developed PrismSNV and Ligo-Seq, a single-cell full-length transcriptome sequencing platform, to quantify transcriptomic displacement associated with within-cell SNV-state toggling. Across 26 samples from three cancer types, more than 60% of candidate SNVs showed significant cell-type-specific displacement with over 30% variation in magnitude. Sequence-based deleteriousness was poorly aligned with cellular displacement, and fewer than 3% of top-displacement SNVs across six tumor types were catalogued in ClinVar. Displacement was strongest in transcriptionally plastic, less differentiated states. Analysis of 655,349 CD4+ T-cell transcriptomes further showed that SNV-gene associations changed in magnitude and sometimes direction during activation. Lack of recurrence or clinical annotation does not imply transcriptomic inertness; variant impact is shaped by cellular context rather than sequence alone, establishing the variant-cell pair as a critical unit for interpreting somatic variation.

genetics↗

Genetic and Epigenetic Landscape of Self-Identified Hispanics/Latino in All Of Us

Human genetic studies still underrepresent many populations, limiting discovery and interpretation of medically relevant variation. Extensive admixture in self-identified Hispanic/Latino populations increases the need for representative reference data and ancestry-aware interpretation of medically relevant variation. We used long-read sequencing to analyze genetic variation, ancestry, and DNA methylation in 1,490 self-identified Hispanic/Latino participants from the All of Us Research Program. We identified 10 million novel variants and more than 100 candidate phenotype associations, with fine-mapping prioritizing structural variants over nearby single-nucleotide variants in more than half. We linked 3,329 tandem repeats to DNA methylation, resolved widespread allele-specific methylation, and identified ancestry-linked regulation across paralogous genes. These results reveal previously inaccessible genetic and regulatory variation and show the value of long-read sequencing for diverse populations.

genetics↗