An international research team led by RIKEN Center for Biosystems Dynamics Research has uncovered a significant genetic mechanism in the roundworm C. elegans, revealing that vital RNA for telomere maintenance does not originate from its own gene but instead hitchhikes within another gene’s intron. This discovery, published in Science, suggests that such DNA hitchhiking may be a widespread evolutionary strategy among animals, with potential implications for anti-aging therapies and regenerative medicine in humans.
Telomeres, essential for protecting chromosome ends, shorten with each cell division, leading to cellular senescence and aging. While somatic cells experience this decline, germ cells maintain telomere length through telomerase, which was previously thought to rely on a specific gene, TERC. The study reveals that C. elegans utilizes a novel intronic long noncoding RNA, termed terc-1, located within the gene nmy-2, to produce telomerase RNA. This unexpected mechanism highlights the adaptability of telomerase regulation and opens avenues for understanding telomere biology and its applications in regenerative health.
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