Abstract
Living at high density and with low genetic diversity are factors that should both increase the susceptibility of organisms to disease. Therefore, group living organisms, especially those that are inbred, should be especially vulnerable to infection and therefore have particular strategies to cope with infection. Phenotypic plasticity, underpinned by epigenetic changes, could allow group living organisms to rapidly respond to infection challenges. To explore the potential role of epigenetic modifications in the immune response to a group-living species with low genetic diversity, we compared the genome-wide DNA methylation profiles of five colonies of social spiders (Stegodyphus dumicola) in their natural habitat in Namibia at the point just before they succumbed to infection to a point at least six months previously where they were presumably healthier. We found increases in genome- and chromosome-wide methylation levels in the CpG, CHG, and CHH contexts, although the genome-wide changes were not clearly different from zero. These changes were most prominent in the CHG context, especially at a narrow region of chromosome, hinting at an as-of-yet unsuspected role of this DNA methylation context in phenotypic plasticity. However, there were few clear patterns of differential methylation at the base level, and genes with a known immune function in spiders had mean methylation changes close to zero. Our results suggest that DNA methylation may change with infection at large genomic scales, but that this type of epigenetic change is not necessarily integral to the immune response of social spiders.
| Original language | English |
|---|---|
| Pages (from-to) | 410–417 |
| Number of pages | 8 |
| Journal | Heredity |
| Volume | 133 |
| Early online date | 12 Sept 2024 |
| DOIs | |
| Publication status | Published - Dec 2024 |
Bibliographical note
We are grateful for the issued permissions to perform field work (permit number 1362/2017 granted by the Ministry of Environment and Tourism in Windhoek, Namibia. We thank those integral to the collection of the field data, especially Tharina Bird, Virginia Settepani, and Tom Tregenza. Two anonymous reviewers provided constructive feedback that helped us improve the manuscript.Data Availability Statement
The raw sequence data are available through NCBI, BioProject ID: PRJNA1131970. The code files for the generation and analysis of the sequences are available at https://figshare.com/s/8ec0f3ee85a1eb0f2f3e.Funding
DF was supported by the Royal Society of Edinburgh (RSE Saltire Early Career Fellowship, grant no. 1940), while TB was supported by The Danish Council for Independent Research (grant no. 0135-443 00201B) and the Novo Nordisk Foundation (Interdisciplinary Synergy grant, grant no. NNF16OC0021110).
| Funders | Funder number |
|---|---|
| Royal Society of Edinburgh | 1940 |
| Independent Research Fund Denmark | 0135- 443 00201B |
| NOVO Nordisk foundation | NNF16OC0021110 |