Maternal glucocorticoids decrease telomere length of sons but not daughters of a wild lizard
The effect of stress-relevant maternal glucocorticoids (e.g. corticosterone, CORT) on offspring phenotype is of interest to the fields of biology, particularly in the face of increasing environmental perturbations. However, little is known about the mechanisms underlying long-term effects of CORT on offspring lifespan. Telomeres, the protective endcaps of chromosomal DNA, could play a role as telomere shortening is associated with disease states and cellular senescence. Here, we use a modified real time quantitative PCR assay protocol to assess telomere length from small amounts of DNA (<60ng); a method that facilitates comparisons across studies. We tested the hypothesis that increased maternal CORT during pregnancy will decrease offspring telomere length, as CORT increases reactive oxygen species generation which can decrease telomere length. While this connection is well established within individuals, it has rarely been examined cross-generationally, especially in non-model systems. We treated wild caught gravid female eastern fence lizards (Sceloporus undulatus) daily with transdermal applications of CORT, at ecologically relevant levels, from capture to laying. Mothers and resulting hatchlings were sampled for DNA. Maternal CORT treatment did not alter maternal telomere length. There was, however, a sex specific effect of maternal CORT on offspring telomeres, explained by a decrease offspring telomere length of sons but not daughters. There was a maternally heritable component to offspring telomere length. The decreased telomere length of sons may be costly and could counteract other potentially adaptive phenotypic changes associated with maternally derived CORT. Further research should explore the fitness consequences of this maternal CORT effect.
|Work Title||Maternal glucocorticoids decrease telomere length of sons but not daughters of a wild lizard|
|Subtitle||Effects of CORT on telomeres|
|License||Public Domain Mark 1.0|
|Deposited||May 31, 2019|
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