​Challenging environmental conditions experienced early in life can be associated with increased mortality and disease risk into adulthood, and telomeres are thought to link early life stress with these later phenotypic effects. Telomeres naturally shorten with age, and higher rates of loss occur earlier in life when cells most rapidly grow and divide. However, telomere loss has been linked with stress exposure, and can be reversed with upregulation of the enzyme telomerase, which is highly expressed in proliferative tissues and rapidly growing individuals. While studies have begun relating telomere dynamics to tissue function and disease, the mechanistic links between telomere dynamics and tissue dysfunction remain largely unknown; in order to answer this question, we must first investigate how telomere dynamics of disease-prone tissues actually respond to stress. ​Therefore, I am interested in how tissues vary in their sensitivity to stress-induced telomere dynamics in tree swallow chicks (Tachycineta bicolor). 

Q. How do tissues vary in their stress-induced telomere loss?

Q. Which tissues are best able to upregulate protection mechanisms (i.e. telomerase) post-stress?
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Q. How flexible is telomere regulation? How quickly does it respond to stress, and how long does the response last? Does flexibility differ between regulatory mechanisms?

My student Keegan getting ready for sample collection in the field.