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Journal of Heredity 2003:94(2)
© 2003 The American Genetic Association 94:181-183

Brief Communication

Programmed Cell Death and Hybrid Incompatibility

S. A. Frank, and C. M. Barr

From the Department of Ecology and Evolutionary Biology, University of California, Irvine, CA 92697-2525, USA.

Address correspondence to S. A. Frank at the address above, or e-mail: safrank{at}uci.edu.

We propose a new theory to explain developmental aberrations in plant hybrids. In our theory, hybrid incompatibilities arise from imbalances in the mechanisms that cause male sterility in hermaphroditic plants. Mitochondria often cause male sterility by killing the tapetal tissue that nurtures pollen mother cells. Recent evidence suggests that mitochondria destroy the tapetum by triggering standard pathways of programmed cell death. Some nuclear genotypes repress mitochondrial male sterility and restore pollen fertility. Normal regulation of tapetal development therefore arises from a delicate balance between the disruptive effects of mitochondria and the defensive countermeasures of the nuclear genes. In hybrids, incompatibilities between male-sterile mitochondria and nuclear restorers may frequently upset the regulatory control of programmed cell death, causing tapetal abnormalities and male sterility. We propose that hybrid misregulation of programmed cell death may also spill over into other tissues, explaining various developmental aberrations observed in hybrids.


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