In U. maydis the multiallelic b locus controls sexual and pathogenic development. In the b locus a gene coding for a regulatory protein had been identified, and it was suggested that the interaction of two b polypeptides specified by different alleles programs sexual development in this fungus. We now demonstrate the existence of a second regulatory gene in the b locus. We term this gene bW and refer to the former as the bE gene. Both genes exist in many alleles. Although unrelated in primary sequence, both genes are similar in their overall organization. The gene products display allele-specific variability in their N-terminal domains, show a high degree of sequence conservation in the C-terminal domains, and contain a homeodomain-related motif. Genetic evidence is provided to show that the pair of bE and bW polypeptides encoded by different b alleles is the key regulatory species.

The processes of aging and photoaging are associated with an increase in cellular oxidation. This may be in part due to a decline in the levels of the endogenous cellular antioxidant coenzyme Q10 (ubiquinone, CoQ10). Therefore, we have investigated whether topical application of CoQ10 has the beneficial effect of preventing photoaging. We were able to demonstrate that CoQ10 penetrated into the viable layers of the epidermis and reduce the level of oxidation measured by weak photon emission. Furthermore, a reduction in wrinkle depth following CoQ10 application was also shown. CoQ10 was determined to be effective against UVA mediated oxidative stress in human keratinocytes in terms of thiol depletion, activation of specific phosphotyrosine kinases and prevention of oxidative DNA damage. CoQ10 was also able to significantly suppress the expression of collagenase in human dermal fibroblasts following UVA irradiation. These results indicate that CoQ10 has the efficacy to prevent many of the detrimental effects of photoaging.

No abstract

Mitochondrial DNA mutations play a major role in human aging processes and degenerative diseases. The most frequently reported marker for mutations of the mitochondrial DNA in human skin is a 4977 bp large-scale deletion, called the Common Deletion. Although this deletion is rarely detectable and constitutes only one example of the multitude of about 50,000 known mutations in mitochondrial DNA, it can represent "the tip of the iceberg" of all types of mitochondrial DNA mutations. We established a quantitative real-time polymerase chain reaction assay to detect the Common Deletion in vitro as well as in vivo/ex vivo. In contrast to previous studies, we were able to demonstrate that the Common Deletion is frequently abundant in keratinocytes isolated from various donors. Quantitative analysis of the mutation indicated interperson variations but obviously no relation to the donors' ages. Prolonged proliferation of keratinocytes led to a distinct reduction in the amount of the Common Deletion. Single ultraviolet A irradiation (12 J per cm2 and 15 J per cm2) neither in vitro nor in vivo increased the incidence of the mutation in keratinocytes, whereas repetitive irradiation resulted in a clear increase in vitro. Again, prolonged cultivation of these irradiated cells caused a significant reduction in the amounts of the deletion. In view of these results, the Common Deletion appears to be a useful marker rather for ultraviolet-A-induced alterations than for chronologic aging in human skin keratinocytes.

Time-distinct gene induction of IL-1beta, TNFalpha and IL-1beta is involved in UV-induced immune reactions, but no considerable changes were found for IL-10r or IL-7.