Cytoplasmic male sterility is a maternally inherited trait that suppresses pollen production due to the interaction of nuclear and mitochondrial genomes. In maize three types of CMS systems, namely CMS-T, CMS-S and CMS-C, have been documented and are differentiated by the reaction to restorers, mitochondrial DNA restriction digest patterns, and complements of low molecular weight plasmids. CMS-T is restored fully by Rf-1 and Rf-2, CMS-S by Rf-3, and CMS-C by Rf-4. All restorer genes except Rf-2 restore fertility by affecting the transcript profile of CMS-associated locus. The sterility is caused by the disorganization of the tapetum and surrounding cell layers as a result of the expression of pollen specific genes. Even though such phenotypes are associated with gene dysfunction in mitochondria, the chloroplasts have emerged as ideal organs for engineering male sterility in crop plants. A number of systems such as barnase-barstar have been standardized in Brassica. Recently, polyhydroxy butyrate was identified as a potential candidate gene for engineering male sterility. Moreover, a broad group of proteins called PPR (pentatricopeptide repeat) proteins has also shown to hold great promise for engineering male sterility in crop plants as most of the restorers belong to this category. In maize one such protein, CRP-1, has been identified.