DRP008925
Does mitochondria fine-tune epigenetic nuclear function?
Plants, particularly challenged by environmental stress, evolved a set of genes to respond to such stress. When individual components of this gene set (for example the receptors for particular pathogen) are over expressed in a transgenic situation, they may significantly alleviate resistance but there is a fitness cost. Intrinsic mechanisms exploiting DNA methylation dynamics may contribute to a balance between resistance and fitness by maintaining moderate expression at multiple resistance genes in a way that it can be quickly induced to higher levels for only a short time needed and switching the gene off again once the stress disappears. Importantly, fitness is not compromised when such a tuner (DNA demethylation enzyme) is in place. However, DNA demethylation itself bears another great cost, namely, genome stability. Because the strong covalent bond between mehylation and DNA cannot be removed, the DNA backbone needs to be cleaved at the site of the base to which methylation is attached. This process is regulated by cofactors named Fe-S clusters. The most upstream component of the Fe-S clusters biogenesis pathway is located in the mitochondria. This project investigates the intriguing possibility that mitochondria fine- tunes nuclear function and the underlying mechanisms.