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This Week in Science: Nov 25, 2011

In this week's issue of Science, Miyuki Sato and Ken Sato from Gunma University in Japan report that autophagy is necessary for the removal of the paternal mitochondria genome in C. elegans. "Autophagosomes engulf paternal mitochondria, resulting in their lysosomal degradation during early embryogenesis," Sato and Sato write, adding that that gives rise to the maternal inheritance of mitochondria.

Similarly, Sara Al Rawi at the Université Pierre et Marie Curie in Paris and her colleagues write in this week's Science that in C. elegans, at fertilization, spermatozoon recruit autophagosomes that degrate the paternal mitochondria.

A related Perspectives article from the University of Texas Southwestern Medical Center's Beth Levine and The Weizmann Institute of Science's Zyulun Elazar notes that "the findings of Sato and Sato and Al Rawi et al. help to explain how paternal mitochondria and mtDNA are destroyed, but why they are destroyed remains a mystery."

Also in this week's Science, researchers led by Dana-Farber Cancer Institute's Anthony Letai report that priming cancer cell mitochondria to the apoptotic threshold affects clinical response to cytotoxic chemotherapy agents. The researchers used BH3 profiling to determine the extent of priming in a number of cancer cell types, as BH3 is needed for mitochondrial cell death. "Here we show that differential mitochondrial priming correlates with, and may be a determinant of, differential chemosensitivity. One implication of these results is that agents that selectively increase priming in cancer cells, even if they do not cause cell death by themselves, might enhance the response of tumors to conventional chemotherapy," the researchers write.

A related Perspectives article from Sanford-Burmhan Medical Research Institute's John Reed says that "whether a prominent role for mitochondrial priming applies for all types of cancer, especially solid tumors, remains to be determined." He adds, though, that "the link established between BH3 peptide–induced mitochondrial priming in vitro and clinical responses to chemotherapy, even if they are only applicable to hematological malignancies, bodes well for the various BH3 mimetic therapeutics currently marching their way through clinical trials."

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