The Caenorhabditis elegans LET‐418/Mi2 plays a conserved role in lifespan regulation. Issue 6 (16th August 2013)

• Record Type: Journal Article
• Authors: De, Véronique; Pfefferli, Catherine; Passannante, Myriam; Belhaj, Khaoula; von, Alina; Sprecher, Simon G.; Müller, Fritz; Wicky, Chantal
• Is Part Of: Aging cell. Volume 12:Issue 6(2013:Dec.)
• Page Start: 1012
• Page End: 1020
• Publication Date: 2013-08-16
• Subjects: Cells -- Aging -- Periodicals; 571.8783605
• DOI: 10.1111/acel.12129
• Languages: English
• ISSNs: 1474-9718

Abstract

<abstract abstract-type="main" id="acel12129-abs-0001"> <title>Summary</title> <p>The evolutionarily conserved nucleosome‐remodeling protein Mi2 is involved in transcriptional repression during development in various model systems, plays a role in embryonic patterning and germ line development, and participates in DNA repair and cell cycle progression. It is the catalytic subunit of the nucleosome remodeling and histone deacetylase (NuRD) complex, a key determinant of differentiation in mammalian embryonic stem cells. In addition, the <italic>Drosophila</italic> and <italic>C. elegans </italic>Mi2 homologs participate in another complex, the MEC complex, which also plays an important developmental role in these organisms. Here we show a new and unexpected feature of the <italic>C. elegans </italic>Mi2 homolog, LET‐418/Mi2. Lack of LET‐418/Mi2 results in longevity and enhanced stress resistance, a feature that we found to be conserved in <italic>Drosophila</italic> and in <italic>Arabidopsis</italic>. The fact that depletion of other components of the NuRD and the MEC complexes did not result in longevity suggests that LET‐418 may regulate lifespan in a different molecular context. Genetic interaction studies suggest that <italic>let‐418</italic> could act in the germ‐cell‐loss pathway, downstream of <italic>kri‐1</italic> and <italic>tcer‐1</italic>. On the basis of our data and on previous findings showing a role for <italic>let‐418</italic> during development, we propose that LET‐418/Mi2 could be part of a system that drives development and reproduction with concomitant life‐reducing effects later in life.</p> </abstract>