Abstract

A model is proposed to account for the features of cytoplasmically inherited male sterility in higher plants. It is suggested that normal anther development is prevented by an interaction between a substance(s) present only in anthers and organelles with altered structures. The alterations in the organelles (mitochondria or chloroplasts) result from mutations in mitochondrial or chloroplast DNA. The involvement of a regulatory substance(s) under developmental control can account for the variation in the extent of sterility in different anthers and the dependence of sterility on the environment. Nuclear fertility restorer genes are postulated to correct the altered organelle structure making the organelles insensitive to the anther substance(s) or to interfere with the production or transport of the anther substance(s). The model, which can be experimentally tested, has been derived from observations that somatic maize mitochondria from certain cytoplasmic male sterile genotypes have altered structures and these altered structures are partially reverted in the presence of nuclear fertility restorer alleles.

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