See February 2007 issue of the Journal of Experimental Biology, "Outside JEB" feature by Graham R. Scott reviews our work: "Mitochondria and Making New Species" J Exp Biol 2007 210:iv-v.
Also notice the mention of our Tigriopus hybrid breakdown work in Science. See News Focus article:
Evolution: "Two Rapidly Evolving Genes Spell Trouble for Hybrids" Elizabeth Pennisi, Science 24 Nov 2006: 1238-1239.
...and published in The American Naturalist Vice Presidential Symposium (Dec 2006):
R.S. Burton, C.K. Ellison, and J.S. Harrison (University of California, San Diego), "The sorry state of F2 hybrids: consequences of rapid mitochondrial DNA evolution in allopatric populations".
Researchers from Scripps Institution of Oceanography have proposed that rapid evolution of the mitochondrial genome may reduce the fitness of interpopulation hybrids during the early stages of speciation. Although matings between individuals from long-isolated population frequently result in offspring that outperform their parents (F1 hybrid vigor), offspring in subsequent generations of interbreeding typically show slower growth and suffer higher mortality than those produced by within-population matings. Thsi general phenomenon underlies much of modern agriculture, where farmers must annually purchase F1 hybrid seed to maximize yield. Why does hybrid vigor breakdown in subsequent generations? Surprisingly little is known about the genes that are responsible for the poor performance of generation (F2) hybrids. In this paper, Burton, Ellison and Harrison suggest that poor hybrid performance results in part from high mutation rates of the small set of genes located in the mitochondrial DNA. These genes encoded components of the biochemical pathway (mitochondrial electron transport system) that provides much of the energy needed by oxygen-breathing organisms. But other critical parts of the pathway are encoded in the more slowly evolving nuclear genome. Within each population are encoded in the more slowly evolving nuclear genome. Within each population nuclear and mitochondrial genes co-evolve,maintaining intricate functional interactions. In F2 hybrids between populations, these interactions may be disrupted, resulting in reduced capacity for generating cellular energy. Laboratory crosses between geographically isolated populations of a marine copepod produce F2 hybrids with reduced fitness. Experiments show that mitochondria isolated from F2 hybrids have reduced capacity for generating energy and that this reduced capacity is correlated with slower growth and decreased survivorship in hybrids. These results support the hypothesis that rapid changes in mitochondrial genes contribute to the sorry state of F2 hybrids.
Also notice the mention of our Tigriopus hybrid breakdown work in Science. See News Focus article:
Evolution: "Two Rapidly Evolving Genes Spell Trouble for Hybrids" Elizabeth Pennisi, Science 24 Nov 2006: 1238-1239.
...and published in The American Naturalist Vice Presidential Symposium (Dec 2006):
R.S. Burton, C.K. Ellison, and J.S. Harrison (University of California, San Diego), "The sorry state of F2 hybrids: consequences of rapid mitochondrial DNA evolution in allopatric populations".
Researchers from Scripps Institution of Oceanography have proposed that rapid evolution of the mitochondrial genome may reduce the fitness of interpopulation hybrids during the early stages of speciation. Although matings between individuals from long-isolated population frequently result in offspring that outperform their parents (F1 hybrid vigor), offspring in subsequent generations of interbreeding typically show slower growth and suffer higher mortality than those produced by within-population matings. Thsi general phenomenon underlies much of modern agriculture, where farmers must annually purchase F1 hybrid seed to maximize yield. Why does hybrid vigor breakdown in subsequent generations? Surprisingly little is known about the genes that are responsible for the poor performance of generation (F2) hybrids. In this paper, Burton, Ellison and Harrison suggest that poor hybrid performance results in part from high mutation rates of the small set of genes located in the mitochondrial DNA. These genes encoded components of the biochemical pathway (mitochondrial electron transport system) that provides much of the energy needed by oxygen-breathing organisms. But other critical parts of the pathway are encoded in the more slowly evolving nuclear genome. Within each population are encoded in the more slowly evolving nuclear genome. Within each population nuclear and mitochondrial genes co-evolve,maintaining intricate functional interactions. In F2 hybrids between populations, these interactions may be disrupted, resulting in reduced capacity for generating cellular energy. Laboratory crosses between geographically isolated populations of a marine copepod produce F2 hybrids with reduced fitness. Experiments show that mitochondria isolated from F2 hybrids have reduced capacity for generating energy and that this reduced capacity is correlated with slower growth and decreased survivorship in hybrids. These results support the hypothesis that rapid changes in mitochondrial genes contribute to the sorry state of F2 hybrids.