Study of molecular coordination between nuclear and mitochondrial replications.

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ATR is highly conserved in all eukaryotes and functions as a cell-cycle nuclear checkpoint kinase. In mammals, ATR hypomorphic mutation causes a complex disease known as Seckel syndrome. However, molecular mechanisms that cause a wide variety of symptoms including accelerated aging have remained unclear. We here found that in the nematode Caenorhabditis elegans, a deletion mutant of ATR atl-1 achieved longevity. Transcription levels of certain superoxide dismutase genes significantly increased in the mutant. In addition, mammalian ATR over-expression induced autophagic cell death.