Cytoplasmic male sterility: Basic mechanism and practical applications

Male sterile lines have great potential for the production of hybrid seeds. Of the various types, cytoplasmic male sterility is easy to maintain and employ. Cytoplasmic male sterility can be induced by several chemicals (Ethyl methane sulphonate, ethidium bromide, streptomycin's, mitomycin, etc.) and is correlated with mit DNA changes. Cytoplasmic male sterility in maize and Petunia is attributed to chimeric genes produced as a consequence of intra mit DNA recombination. Chimeric genes give rise to protein(s) which degenerate tapetal cells prematurely causing pollen abortion. In some instances product of chimeric gene causes premature dissolution of callose wall leading to disintegration of developing microspores. In oilseed rape, male sterile transgenic plants have been raised through the use of chimeric TA29-barnase gene, whereas in tobacco chimeric, callase gene has been used to induce male sterility. Through T A-29-barstar gene, male fertility has been restored in oilseed rape. Genetic engineering of anther-specific expression of the rot B gene of Agrobacterium rhizogenes increased IAA content in anthers and altered the anther development leading to male sterility. Recent work has shown that antisense of flavonoid biosynthesis in Petunia anthers resulted in male sterility. Growth hormones like ABA are also implicated. Some workers have obtained a dominant genetic male sterility trait through transformation in Brassica napus and consisted of ribonuclease gene under the control of a tapetum specific promoter. The future prospects of raising male sterile lines and their practical uses are further discussed.