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A fln-2 mutation affects lethal pathology and lifespan in C. elegans

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  • Yuan Zhao

    (University College London)

  • Hongyuan Wang

    (University College London
    Harbin Institute of Technology)

  • Richard J. Poole

    (University College London)

  • David Gems

    (University College London)

Abstract

Differences in genetic background in model organisms can have complex effects on phenotypes of interest. We previously reported a difference in hermaphrodite lifespan between two wild-type lines widely used by C. elegans researchers (N2 hermaphrodite and male stocks). Here, using pathology-based approaches and genome sequencing, we identify the cause of this difference as a nonsense mutation in the filamin gene fln-2 in the male stock, which reduces early mortality caused by pharyngeal infection. We show how fln-2 variation explains previous discrepancies involving effects of sir-2.1 (sirtuin deacetylase) on ageing, and show that in a fln-2(+) background, sir-2.1 over-expression causes an FUDR (DNA synthesis inhibitor)-dependent reduction in pharyngeal infection and increase in lifespan. In addition we show how fln-2 variation confounds effects on lifespan of daf-2 (insulin/IGF-1 signalling), daf-12 (steroid hormone signalling), and eat-2 (putative dietary restriction). These findings underscore the importance of identifying and controlling genetic background variation.

Suggested Citation

  • Yuan Zhao & Hongyuan Wang & Richard J. Poole & David Gems, 2019. "A fln-2 mutation affects lethal pathology and lifespan in C. elegans," Nature Communications, Nature, vol. 10(1), pages 1-10, December.
    • Handle: RePEc:nat:natcom:v:10:y:2019:i:1:d:10.1038_s41467-019-13062-z
    DOI: 10.1038/s41467-019-13062-z
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