Indian Journal of Genetics and Plant Breeding (The)
SCOPUSWeb of Science
  • Year: 1985
  • Volume: 45
  • Issue: 3

Mobile Genes of Mitochondria and Cytoplasmic Male Sterility

  • Author:
  • H. K. Srivastava1,
  • Total Page Count: 33
  • Page Number: 447 to 479

1Central Institute of Medicinal and Aromatic Plants, Post Bag No. 1, P.O. RSM Nagar, Lucknow, 226 016

*Department of Biotechnology, (ICGEB CELL) M/o Science & Technology, CGO Complex, Lodhi Road. Block No. 2, 7th Floor, New Delhi, 110 003

Abstract

A list of crop plants with data on genetic determinants of cytoplasmic male sterility associated with mitochondria, chloroplast, plasmid-like DNAs or extrachromosomal elements, and RNA virus-like agents has been compiled. Several distinct lines of evidence suggest that genes which control staminal sterility in maize, sorghum, sugarbeet, and wheat are located on mtDNA and not on ctDNA. The classical division of maize and sorghum cytoplasms into distinct subgroups correlates well with restriction patterns of mtDNA. Plasmid DNAs such as SI (6.2 kb linear) and S2 (5.2 kb linear) within maize mitochondria in CMS-S line comport-like transposable elements as they appear to jump in and out of the mitochondria] genome. A theory is construed according to which mitochondrial plasmid DNAs are entrusted with the role of vectors for mobile gene (s) of staminal sterility. Relevant points in support of a mobile gene hypothesis, i.e., genes with the flexibility to become integrated into mitochondrial and nuclear genomes in one or other forms of male sterility are discussed. Whether plasmid DNAs as molecular vectors for fertility/sterility genes are transposed from one intracellular location to another as mobile genes and whether such integration takes place at different loci in the mitochondrial and/or nuclear genome during reversions still remains to be ascertained. All this opens up extraordinary prospects for unravelling the precise molecular mechanism of staminal sterility in crop plants. The recently established concept of the fluidity (flexibility/mobility) of the eukaryotic genome structure (the case of the jumping genes and especifically "split genes" in both nucleus and mitochondria) and the relevance of such mobile genes in determination of staminal sterility, either purely cytoplasmic (mitochondrial chromosome) or nuclear (nuclear chromosome) or combined (intergenomic interaction), can be viewed as important innovations in plant genetics. Further observations on DNA sequencing of unique genes of the plant mitochondrial systems provide convincing evidence for alteration of mitochondrial genome to be the major cause of CMS. Plasmid DNAs are natural components of mitochondrial genomes and they can be activated for transposition by genomic stress. The results presented here suggest that transfer of the male sterility gene from the nuclear to the mitochondrial genome, or vice versa, may have occurred in the course of evolution. The mobile gene concept confers molecular explanation for earlier observations of conventional genetical and breeding experiments in which various causes and factors were held responsible for the occurrence of one or other form of male sterility.