|Gobelman Werner, Karin|
|Holmes, Jennifer - IOWA STATE UNIVERSITY|
|Deqing, Pei - IOWA STATE UNIVERSITY|
Submitted to: Plant Genome Conference Proceedings
Publication Type: Abstract Only
Publication Acceptance Date: January 16, 2002
Publication Date: N/A
Technical Abstract: T-cytoplasm maize (cms-T) has been developed as a model to study the molecular mechanisms underlying mitochondrial transcript processing and restoration of fertility in cytoplasmic male-sterile systems. Male sterility in cms-T results from the function of T-urf13, a T-cytoplasm specific, mitochondrial gene. Nuclear-directed modification of T-urf13 transcripts is mediated by Rf1, Rf8, or Rf*, which in combination with Rf2 suppress the male-sterile phenotype. Rf1 is positioned near the centromere on chromosome 3, whereas Rf8 and Rf* are clustered together on 2L. This position on 2L also harbours Rf3, another nuclear gene that modifies mitochondrial transcripts, but its action is specific to S-cytoplasm maize. Computational analysis of a candidate Rf1 cDNA was used to provide clues as to its possible function. Twenty-six residues of the predicted amino acid sequence revealed 96% similarity with mammalian small nuclear ribonucleoprotein E (snRNP E). The snRNP E protein is an 11-kD basic protein integral to RNA processing reactions and is one of four core proteins associated with the snRNAs of the U (uridine rich) family (U1, U2, U4, U5, and U6). U1 snRNA is initially bound to the 5'-splice site and is released upon recruitment of U4/U5/U6, a process that is consistent with the molecular phenotype of Rf1. Research funded by USDA-NRI OEP 1999-01334.