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The origin of germ cells of Asterina pectinifera was traced back to the posterior enterocoel (PE) of 2-day bipinnaria by two steps. First, the cellular cluster, composed of presumptive germ cells in the coelomic epithelium at brachiolaria stage, was confirmed to be the origin of the aboral haemal sinus located near the hydroporic canal (HC-AHS) by continuous observation of the formation process of HC-AHS. Second, the origin of the cluster was traced back to the PE of 2-day bipinnaria by comparison of the number of the presumptive germ cells in microsurgically PE-removed bipinnariae with that of non-operated control larvae. A summary of the differentiation of germ cells in Asterina pectinifera is given/presented.

The origin of the germ cells and the development of the genital system in the annually spawning starfish, Asterina pectinifera, were studied by light and electron microscopy. Characteristic germ cells were first characterized in gonads after spawning: the gonia are larger than somatic cells, have large nuclei (with electron-lucent nucleoplasm), and show mitochondrial aggregation associated with nuage (electron-dense bodies). In young starfish without gonads similar cells were detected in the haemal sinus, where they were termed primordial germ cells (PGCs). Brachiolariae and metamorphosed juveniles had a cellular cluster in the coelomic epithelium, near the hydroporic canal. The cluster was comprised of cells endowed with the above-mentioned characteristics of the germ cells. The germ cell counts indicated that PGCs migrate from the aboral haemal sinus near the hydroporic canal, through the haemal sinus to the gonads, where they settle, proliferate, and differentiate into gonia.

Rhodotorula glutinis IFO1125 was found to acquire increased aluminium (Al) resistance from 50 microM to more than 5 mM by repetitive culturing with stepwise increases in Al concentration at pH 4.0. To investigate the mechanism underlying this novel phenomenon, wild-type and Al-resistant cells were compared. Neither cell type accumulated the free form of Al (Al(3+)) added to the medium. Transmission electron microscopic analyses revealed a greater number of mitochondria in resistant cells. The formation of small mitochondria with simplified cristae structures was observed in the wild-type strain grown in the presence of Al and in resistant cells grown in the absence of Al. Addition of Al to cells resulted in high mitochondrial membrane potential and concomitant generation of reactive oxygen species (ROS). Exposure to Al also resulted in elevated levels of oxidized proteins and oxidized lipids. Addition of the antioxidants alpha-tocopherol and ascorbic acid alleviated the Al toxicity, suggesting that ROS generation is the main cause of Al toxicity. Differential display analysis indicated upregulation of mitochondrial genes in the resistant cells. Resistant cells were found to have 2.5- to 3-fold more mitochondrial DNA (mtDNA) than the wild-type strain. Analysis of tricarboxylic acid cycle and respiratory-chain enzyme activities in wild-type and resistant cells revealed significantly reduced cytochrome c oxidase activity and resultant high ROS production in the latter cells. Taken together, these data suggest that the adaptive increased resistance to Al stress in resistant cells resulted from an increased number of mitochondria and increased mtDNA content, as a compensatory response to reduced respiratory activity caused by a deficiency in complex IV function.