Characterizing transcriptomic responses to sediment stress across location and morphology in reef-building corals.

Anthropogenic activities increase sediment suspended in the water column and deposition on reefs can be largely dependent on colony morphology. Massive and plating corals have a high capacity to trap sediments, and active removal mechanisms can be energetically costly. Branching corals trap less sediment but are more susceptible to light limitation caused by suspended sediment. Despite deleterious effects of sediments on corals, few studies have examined the molecular response of corals with different morphological characteristics to sediment stress. To address this knowledge gap, this study assessed the transcriptomic responses of branching and massive corals in Florida and Hawai'i to varying levels of sediment exposure. Gene expression analysis revealed a molecular responsiveness to sediments across species and sites. Differential Gene Expression followed by Gene Ontology (GO) enrichment analysis identified that branching corals had the largest transcriptomic response to sediments, in developmental processes and metabolism, while significantly enriched GO terms were highly variable between massive corals, despite similar morphologies. Comparison of DEGs within orthogroups revealed that while all corals had DEGs in response to sediment, there was not a concerted gene set response by morphology or location. These findings illuminate the species specificity and genetic basis underlying coral susceptibility to sediments.

Short-term elevations in glucocorticoids do not alter telomere lengths: A systematic review and meta-analysis of non-primate vertebrate studies.

BACKGROUND: The neuroendocrine stress response allows vertebrates to cope with stressors via the activation of the Hypothalamic-Pituitary-Adrenal (HPA) axis, which ultimately results in the secretion of glucocorticoids (GCs). Glucocorticoids have pleiotropic effects on behavior and physiology, and might influence telomere length dynamics. During a stress event, GCs mobilize energy towards survival mechanisms rather than to telomere maintenance. Additionally, reactive oxygen species produced in response to increased GC levels can damage telomeres, also leading to telomere shortening. In our systematic review and meta-analysis, we tested whether GC levels impact telomere length and if this relationship differs among time frame, life history stage, or stressor type. We hypothesized that elevated GC levels are linked to a decrease in telomere length. METHODS: We conducted a literature search for studies investigating the relationship between telomere length and GCs in non-human vertebrates using four search engines: Web of Science, Google Scholar, Pubmed and Scopus, last searched on September 27th, 2020. This review identified 31 studies examining the relationship between GCs and telomere length. We pooled the data using Fisher's Z for 15 of these studies. All quantitative studies underwent a risk of bias assessment. This systematic review study was registered in the Open Science Framework Registry (https://osf.io/rqve6). RESULTS: The pooled effect size from fifteen studies and 1066 study organisms shows no relationship between GCs and telomere length (Fisher's Z = 0.1042, 95% CI = 0.0235; 0.1836). Our meta-analysis synthesizes results from 15 different taxa from the mammalian, avian, amphibian groups. While these results support some previous findings, other studies have found a direct relationship between GCs and telomere dynamics, suggesting underlying mechanisms or concepts that were not taken into account in our analysis. The risk of bias assessment revealed an overall low risk of bias with occasional instances of bias from missing outcome data or bias in the reported result. CONCLUSION: We highlight the need for more targeted experiments to understand how conditions, such as experimental timeframes, stressor(s), and stressor magnitudes can drive a relationship between the neuroendocrine stress response and telomere length.