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

FEBS Letters

Pring, Daryl R.¹  Howad, Werner²  Kempken, Frank² 

[1] Crop Genetics and Environment Research Unit, USDA-ARS, Department of Plant Pathology and Plant Molecular and Cellular Biology Program, University of Florida, Gainesville, FL 32611, USA;Lehrstuhl für Allgemeine Botanik, Ruhr-Universität Bochum, D44780 Bochum, Germany

关键词: Cytoplasmic male sterility;    Mitochondrial mutation;    RNA editing;    Mitochondrial dysfunction;    Pollen fertility;   

DOI  :  10.1016/S0014-5793(98)01538-5

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 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.

【 授权许可】

Unknown