A mitochondrial gene is lost via homologous recombination during reversion of CMS T maize to fertility.

The Texas (T) male sterile cytoplasm of maize is distinguished by a mitochondrially synthesized 13-kd polypeptide and a high susceptibility to the toxin produced by the fungal pathogen Helminthosporium maydis. Fertile, toxin-resistant revertants show an altered restriction profile for mitochondrial DNA and do not produce the 13-kd polypeptide. Characterization of cosmid clones from CMS T maize and a revertant shows that a heavily transcribed open reading frame named T-URF13, potentially coding a 13-kd product, is deleted in the revertant mitochondria. Six transcripts present in CMS T mitochondria, 4000, 3000, 2000, 1800, 1500 and 1200 nucleotides in length, are lacking in revertant mitochondria. T-URF25, an open reading frame coding for a 25-kd product, lies to the 3' end of T-URF13 but is retained in the revertants. T-URF13 and T-URF25 are co-transcribed in CMS T mitochondria; in the revertant T-URF25 is present on a 3100-nucleotide species. The recombination that caused these changes involved a 127-bp repeated sequence. Homologous recombination took place within the central 55 bp of this imperfect repeat. Hybridization analysis of DNA and RNA from other revertants demonstrates that a similar or identical event has taken place independently in these revertants.