Title: MUTATIONS AT SPECIFIC ATP6 CODONS WHICH CAUSE HUMAN MITOCHONDRIAL DISEASES ALSO LEAD TO MALE STERILITY IN A PLANT.
Kempken, Frank - RUHR UNIV, GERMANY
Howad, Werner - RUHR UNIV, GERMANY
Submitted to: Journal of Federation of American Societies for Experimental Biology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: November 11, 1998
Publication Date: N/A
Interpretive Summary: RNA editing is a process that occurs in plants wherein the genetic code as found on DNA is changed when the DNA is transcribed into a messenger RNA (mRNA). mRNA is the molecule that directs the production of proteins. RNA editing has been found to be required for many mRNAs to ensure the production of a functional protein. Cytoplasmic male sterility is a trait of higher plants wherein pollen production is interrupted, resulting in male-sterile plants. This trait has been assigned to the mitochondrion, a cellular organelle associated with energy production. Scientists at USDA, ARS, Gainesville, FL found that the mitochondrial gene atp6 requires editing in sorghum, but that the gene is not edited in young pollen grains of male-sterile plants. Genes that restore male fertility result in atp6 mRNAs that are correctly edited. Two of the points at which editing is required in sorghum atp6 have been found to be mutated in two mitochondrial diseases of humans. Therefore, we propose a hypothesis wherein absence of editing in young sorghum pollen may mimic these human diseases and results in a non-functional atp6, leading to pollen death. Experimental evidence that would prove the hypothesis may lead to hard evidence of one basis of male sterility in sorghum.
Defects in the human mitochondrial genetic system result in some diseases. These disorders are the result of rearrangements or point mutations in mitochondrial genes. In higher plants mutations and rearrangements in the mitochondria DNA are believed to cause cytoplasmic male sterility (CMS), a mitochondrially inherited inability to produce viable pollen. In sorghum, formation of CMS is strongly correlated with anther-specific loss of mitochondrial atp6 RNA editing. Here we show that this loss of atp6 RNA editing mimics point mutations at codons that cause severe disorders in humans. We conclude that (i) loss of RNA editing in sorghum anthers probably causes CMS, (ii) similarities exist in the onset of mitochondrial dysfunction in plant and human tissues, and (iii) the evolutionary appearance of RNA editing provided a mechanism to compensate for otherwise lethal point mutations.