Ecologists and evolutionary biologists have been looking for the key(s) to the success of scyphomedusae through their long evolutionary history in multiple habitats. Their ability to generate young medusae (ephyrae) via two distinct reproductive strategies, strobilation or direct development from planula into ephyra without a polyp stage, has been a potential explanation. In addition to these reproductive modes, here we provide evidence of a third ephyral production which has been rarely observed and often confused with direct development from planula into ephyra. Planulae of
Longevity plays a key role in the fitness of organisms, so understanding the processes that underlie variance in senescence has long been a focus of ecologists and evolutionary biologists. For decades, the performance and ultimate decline of mitochondria have been implicated in the demise of somatic tissue, but exactly why mitochondrial function declines as individual’s age has remained elusive. A possible source of decline that has been of intense debate is mutations to the mitochondrial DNA. There are two primary sources of such mutations: oxidative damage, which is widely discussed by ecologists interested in aging, and mitochondrial replication error, which is less familiar to most ecologists. The goal of this review is to introduce ecologists and evolutionary biologists to the concept of mitochondrial replication error and to review the current status of research on the relative importance of replication error in senescence. We conclude by detailing some of the gaps in our knowledge that currently make it difficult to deduce the relative importance of replication error in wild populations and encourage organismal biologists to consider this variable both when interpreting their results and as viable measure to include in their studies.
- Publication Date:
- NSF-PAR ID:
- 10116831
- Journal Name:
- Integrative and Comparative Biology
- Volume:
- 59
- Issue:
- 4
- Page Range or eLocation-ID:
- p. 970-982
- ISSN:
- 1540-7063
- Publisher:
- Oxford University Press
- Sponsoring Org:
- National Science Foundation
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