Cytoplasmic male sterility is total or partial male sterility in plants as the result of specific nuclear and interactions. Male sterility is the failure of plants to produce functional anthers, pollen, or male gametes.
The first documentation of male sterility was by Joseph Gottlieb Kölreuter, who observed anther abortion within species and specific hybrids. Cytoplasmic male sterility (CMS) has now been identified in over 150 plant species. It is more prevalent than female sterility, either because the male sporophyte and gametophyte are less protected from the environment than the ovule and embryo sac, or because it results from natural selection on mitochondrial genes which are maternally inherited and are thus not concerned with pollen production. Male sterility is easy to detect because a large number of pollen grains are produced and are easily studied. Male sterility is assayed through staining techniques (carmine, lactophenol or iodine), while detection of female sterility is by the absence of seeds. Male-sterile plants may be propagated, since they can still set seed, while female-sterile plants cannot. Male sterility can arise spontaneously via mutations in nuclear genes and/or cytoplasmic genes.
Male sterility can be either cytoplasmic or cytoplasmic–genetic. CMS is caused by the extranuclear genome ( or chloroplast) and shows maternal inheritance. Manifestation of male sterility in CMS may be controlled either entirely by cytoplasmic factors or by interaction between cytoplasmic and nuclear factors.
Cytoplasmic male sterility, as the name indicates, is under extranuclear genetic control (under control of the mitochondrial or plastid genomes). It shows non-Mendelian inheritance, with male sterility inherited maternally. In general, there are two types of cytoplasm: N (normal) and aberrant S (sterile) cytoplasms. These types exhibit reciprocal differences.