The organization and functions of genetic systems controlling cytoplasmic male sterility (CMS) in plants are reviewed. Mitochondrial genes that code for specific proteins disturbing the functions of mitochondria have been found by comparisons between CMS lines and fertile F1 hybrids and between forms originating from in vitro cultures (fertile revertants, cybrids). Nuclear fertility-restorer genes abrogate expression of these mitochondrial genes at the transcriptional or posttranslational level and thereby prevent synthesis of their protein products. A high mutability of the mitochondrial genome in cells cultured in vitro results in the elimination or reorganization of CMS-associated mitochondrial genes or in new mutations causing CMS. Several biotechnological methods are considered with respect to their applicability in identifying and transferring CMS-associated genes and in constructing new CMS forms.

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