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A mitochondrial gene is lost via homologous recombination during reversion of CMS T maize to fertility
Author(s) -
Rottmann W. H.,
Brears T.,
Hodge T. P.,
Lonsdale D. M.
Publication year - 1987
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1002/j.1460-2075.1987.tb02398.x
Subject(s) - biology , plant breeding , molecular genetics , molecular breeding , genetics , library science , gene , botany , computer science
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.