Mutations at specific atp6 codons which cause human mitochondrial diseases also lead to male sterility in a plant

被引:16
作者
Kempken, F [1 ]
Howad, W
Pring, DR
机构
[1] Ruhr Univ Bochum, Lehrstuhl Allgemeine Bot, D-44780 Bochum, Germany
[2] Univ Florida, Dept Plant Pathol, USDA ARS, Crop Genet & Environm Res Unit, Gainesville, FL 32611 USA
[3] Univ Florida, Plant Mol & Cellular Biol Program, Gainesville, FL 32611 USA
关键词
cytoplasmic male sterility; mitochondrial mutation; RNA editing; mitochondrial dysfunction; pollen fertility;
D O I
10.1016/S0014-5793(98)01538-5
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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 mitochondrial 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. (C) 1998 Federation of European Biochemical Societies.
引用
收藏
页码:159 / 160
页数:2
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