Speciation through cytonuclear incompatibility: Insights from yeast and implications for higher eukaryotes

Several features of the yeast mitochondrial genome, including high mutation rate, dynamic genomic structure, small effective population size, and dispensability for cellular viability, make it a promising candidate for generating hybrid incompatibility and driving speciation. Cytonuclear incompatibility, a specific type of Dobzhansky‐Muller genetic incompatibility caused by improper interactions between mitochondrial and nuclear genomes, has previously been observed in a variety of organisms, yet its role in speciation remains obscure. Recent studies in Saccharomyces yeast species provide a new insight, with experimental evidence that cytonuclear incompatibility and DNA sequence divergence are both causes of the reproductive isolation of different yeast species. Interestingly, these two mechanisms seem to be perfectly complementary to each other in terms of their effects and evolutionary trajectories. Direct molecular analyses of the incompatible genes in yeasts have started to shed light on the evolutionary forces driving speciation. Editor's suggested further reading in BioEssays The cytoplasmic structure hypothesis for ribosome assembly, vertical inheritance, and phylogeny Abstract Mitochondrial bioenergetics as a major motive force of speciation Abstract     

Chromosome analysis on two long-term established human colorectal carcinoma cell lines

A chromosomal analysis was carried out on two colorectal carcinoma cell lines (WiDr and COLO 205), which were established 15-20 years ago in the US and were collected by the Cell Bank of the Veterans General Hospital in Taipei. Among the 200 cells counted, 65.5% of WiDr (male) had 68-73 chromosomes, while 74% of the COLO 205 (female) had 70-76 chromosomes per cell. The Y chromosome was absent in the 30 WiDr metaphases analyzed. None of the other chromosomes, including X and the autosomes of both WiDr and COLO 205, revealed such a numerical deficiency. Over half of the autosomes had an average number per cell above 2.0. The existence of 5 or 6 normal homologues for certain autosomes was not rare in either line. Numerous structural abnormal marker chromosomes were present in the cells. As compared with the original chromosome findings which were done over 10 years ago, we noted that the range of chromosome counts was wider and the number of marker chromosomes increased in these long-term cultivated cell lines.