Mitochondria, sex, and mortality.

It has been proposed that prior to the evolution of sex, the endosymbiotic relationship between mitochondria and nuclear genomes would have selected mechanisms that maintained the optimum interaction between the two genomes. Once sex evolved, mating would introduce different, competitive, mtDNA and/or nDNA gene products that could well upset the balance. Mechanisms, such as the specific degradation of one mitochondrial genome that is known to occur, could have been selected to prevent part of such competition. Unlike most protein complexes in the cell, the proteins of the multienzyme complexes of the ox-phos system are derived from both nuclear-genome-coded genes and mitochondrial-genome-coded genes. Minor mutations in either mtDNA or nDNA coding for these proteins are known to lead to major and catastrophic diseases of humans, suggesting that very tight and precise interactions are required. To maintain the evolutionarily established balance after mating, monoallelic expression of the nuclear-coded genes would be advantageous and prevent subtly different competitive proteins from interacting with the resident mitochondria. This would require regulation of the expression of those specific nuclear genes, possibly under the control of the resident mitochondria. It is possible that aging cells could lose the requisite tight regulation and allow expression of proteins derived from the formerly repressed nuclear alleles that would compete for mitochondrial complex sites. With age, random failure of this control could lead to increasingly inefficient mitochondria in different tissues and organs and eventually to senescence and death.

Tagging and localization of a phospholipase D gene in Coprinellus congregatus by restriction enzyme-mediated integration and pulsed-field gel electrophoresis.

We have identified a phospholipase D gene (pld) fragment from a transformant generated by restriction enzyme-mediated integration in Coprinellus congregatus, which is a mushroom-forming basidiomycete. A fragment of pld of this fungus has been cloned from a transformant by gene tagging. The transformation vector has been inserted into pld and this has resulted in a decreased enzyme activity of the transformant compared with the wild strain. C. congregatus has seven chromosomes, the range of its genome size is 1.6-4.7 Mb and pld is located at chromosome 4 where the transformation vector has been inserted.

DNA tests in prolific sheep from eight countries provide new evidence on origin of the Booroola (FecB) mutation.

Recent discoveries that high prolificacy in sheep carrying the Booroola gene (FecB) is the result of a mutation in the BMPIB receptor and high prolificacy in Inverdale sheep (FecX(I)) is the result of a mutation in the BMP15 oocyte-derived growth factor gene have allowed direct marker tests to be developed for FecB and FecX(I). These tests were carried out in seven strains of sheep (Javanese, Thoka, Woodlands, Olkuska, Lacaune, Belclare, and Cambridge) in which inheritance patterns have suggested the presence of major genes affecting prolificacy and in the prolific Garole sheep of India, which have been proposed as the ancestor of Australian Booroola Merinos. The FecB mutation was found in the Garole and Javanese sheep but not in Thoka, Woodlands, Olkuska, Lacaune, Belclare, and Cambridge sheep. None of the sheep tested had the FecX(I) mutation. These findings present strong evidence to support historical records that the Booroola gene was introduced into Australian flocks from Garole (Bengal) sheep in the late 18th century. It is unknown whether Javanese Thin-tailed sheep acquired the Booroola gene directly from Garole sheep from India or via Merinos from Australia. The DNA mutation test for FecB will enable breeding plans to be developed that allow the most effective use of this gene in Garole and Javanese Thin-tailed sheep and their crosses.