Submitted to: Maize Genetics Conference Abstracts
Publication Type: Abstract only
Publication Acceptance Date: 3/1/2007
Publication Date: 4/1/2007
Publication URL: http://www.maizegdb.org/cgi-bin/displayrefrecord.cgi?id=1079486
Citation: Kamps, T.L., Zhao, L., Chamusco, K., Read, V., Anderson, A., Hannah, C., Mccarty, D., Gabay-Laughnan, U., Chase, C. 2007. Molecular Genetics of Mitochondrial Biogenesis in Maize. Maize Genetics Conference Abstracts. Vol 49. p. 95 Interpretive Summary: None.
Technical Abstract: The mitochondrial genome encodes proteins essential for mitochondrial respiration and ATP synthesis. Nuclear gene products, however, are required for the expression of mitochondrial genes and the elaboration of functional mitochondrial protein complexes. We are exploiting a unique collection of maize lines developed from plants selected for nuclear mutations disrupting mitochondrial functions to understand how the nuclear genome contributes to mitochondrial biogenesis and function in plants. These mutations gametophytically restore male fertility to plants with the mitochondrial-encoded, cytoplasmic male sterility trait type S (CMS-S). Although restorer mutations rescue CMS-S pollen function, many are homozygous lethal for maize kernel development. The functions that these nuclear restorer gene products normally perform in mitochondrial biogenesis were investigated by assaying mitochondrial RNA and protein accumulation in starch-filling pollen collected from normal (N)-cytoplasm plants and CMS-S plants carrying seven independent restorer mutations. Two mechanisms for fertility restoration are suggested by the results of these assays. Five unlinked restorer mutations conditioned global loss of mitochondrial gene products through post-transcriptional mechanisms. These restorer mutations are hypothesized to effect fertility by also conditioning the loss of the mitochondrial gene product responsible for CMS-S. Restorer mutations having no obvious effects on mitochondrial gene expression are thought to disrupt mitochondrial-signaled cell death events associated with pollen collapse. Assays for both mechanisms of fertility restoration are under development. To further elucidate the nature of fertility restorer genes and their functions, we are also pursuing molecular cloning strategies. Fifty independent, Mutator (Mu) transposon-induced, seed-lethal mutants were tested by seed phenotype for allelism with the above described seven restorer mutants. Twenty-two independent,Mu transposon-induced, seed-lethal mutants were directly tested for fertility restoration in S-cytoplasm. Nine of the 22 mutants restored fertility to CMS-S plants. These nine mutants were intercrossed to test for allelism. The molecular analysis and allelism test results will be presented.