Generation of a stable folding intermediate which can be rescued by the chaperonins GroEL and GroES

Pig heart mitochondrial malate dehydrogenase was chemically denatured in guanidine HCl. Upon 50-fold dilution of the denaturant spontaneous refolding could be observed in the temperature range 12–32°C. At 36°C spontaneous refolding was not observed but a stable folding intermediate that is fairly resistant to aggregation was formed. This intermediate is readily refolded by the chaperonins GroEL and GroES and may prove useful in future attempts to describe several aspects of chaperonin action at physiological temperatures

Heat-Shock Proteins of Barley Mitochondria and Chloroplasts - Identification of Organellar Hsp-10 and Hsp-12 - Putative Chaperonin-10 Homologs

AbstractTissue slices from barley seedlings were subjected to heat shock and metabolically labelled with [35S]methionine and [35S]lcysteine, Mitochondria and chloroplasts were isolated and shown to contain two novel heat shock proteins of 10 and 12 kDa, respectively. The possibility that these proteins, like a mitochondrial 10 kDa stress protein recently isolated from rat hepatoma cells [(1992) Proc. Natl. Acad. Sci. 89, in press] represent eukaryotic chaperonin 10 homologues is discussed

Somatic mutation rates scale with lifespan across mammals.

The rates and patterns of somatic mutation in normal tissues are largely unknown outside of humans1-7. Comparative analyses can shed light on the diversity of mutagenesis across species, and on long-standing hypotheses about the evolution of somatic mutation rates and their role in cancer and ageing. Here we performed whole-genome sequencing of 208 intestinal crypts from 56 individuals to study the landscape of somatic mutation across 16 mammalian species. We found that somatic mutagenesis was dominated by seemingly endogenous mutational processes in all species, including 5-methylcytosine deamination and oxidative damage. With some differences, mutational signatures in other species resembled those described in humans8, although the relative contribution of each signature varied across species. Notably, the somatic mutation rate per year varied greatly across species and exhibited a strong inverse relationship with species lifespan, with no other life-history trait studied showing a comparable association. Despite widely different life histories among the species we examined-including variation of around 30-fold in lifespan and around 40,000-fold in body mass-the somatic mutation burden at the end of lifespan varied only by a factor of around 3. These data unveil common mutational processes across mammals, and suggest that somatic mutation rates are evolutionarily constrained and may be a contributing factor in ageing