No abstract

In a global transcriptome analysis of three natural and three manipulated honeybee worker phenotypes at different ages, we have investigated the distribution of investment in somatic maintenance of the fat body. Gene expression is modulated so that the bees are able to resist the most life-threatening challenges at the actual life stage. Different modes of maintenance and repair are regulated, apparently to meet the environmental challenges most detrimental to survival and reproductive potential for the hive. We observed a broad down-regulation of genomic and cellular maintenance in the short-lived foragers and nurse bees compared to the long-lived winter bees. Our results show that survival and reproduction of the entire hive is given priority over the individual bees, hence supporting the idea of the honeybee society as a superorganism. Our results also fit the disposable soma theory of aging.

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The AAG family of 3-methyladenine DNA glycosylases was initially thought to be limited to mammalian cells, but genome sequencing efforts have revealed the presence of homologous proteins in certain prokaryotic species as well. Here, we report the first molecular characterization of a functional prokaryotic AAG homologue, i.e. YxlJ, termed bAag, from Bacillus subtilis. The B. subtilis aag gene was expressed in Escherichia coli, and the protein was purified to homogeneity. As expected, B. subtilis Aag was found to be a DNA glycosylase, which releases 3-alkylated purines and hypoxanthine, as well as the cyclic etheno adduct 1,N 6 -ethenoadenine from DNA. However, kinetic analysis showed that bAag removed hypoxanthine much faster than human AAG with a 10-fold higher value for k cat , whereas the rate of excision of 1, N 6 -ethenoadenine was found to be similar. In contrast, it was found that bAag removes 3-methyladenine and 3-methylguanine ϳ10 -20 times more slowly than human AAG, and there was hardly any detectable excision of 7-methylguanine. It thus appears that bAag has a minor role in the repair of DNA alkylation damage and an important role in preventing the mutagenic effects of deaminated purines and cyclic etheno adducts in Bacillus subtilis.Exposure of genomes to a variety of reactive intracellular metabolites and environmental agents results in chemical modifications of the DNA nucleobases, including oxidations, alkylations, and deaminations. Such DNA lesions are primarily repaired through the base excision repair pathway (BER). The first step of BER involves N-glycosylic cleavage of the basesugar bonds by damage-specific DNA glycosylases. The abasic site is cleaved by apurinic/apyrimidinic endonucleases or apurinic/apyrimidinic lyases, and repair is completed through a sequential action of a phosphodiesterase, a DNA polymerase, and a DNA ligase (reviewed in Refs. 1 and 2).Alkylating agents represent one of the most abundant classes of mutagenic and genotoxic agents present in the environment. Repair of alkylation damage is initiated by DNA glycosylases, referred to as 3-methyladenine (3mA) 1 DNA glycosylases, because 3mA is a major substrate for these enzymes.