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Another Californian, a biologist, Cynthia Kenyon, made mutant worms live twice as long as normal -- four weeks instead of two -- by fiddling with genes and hormones.
doi: 10.7554/eLife.07836 Image Some mutant worms live longer than wildtype worms Germ line tissue – the tissue that produces egg and sperm cells – is known to influence the lifespans of several animal species (Kenyon, 2010).
clk-1 mutant worms live longer than their WT counterparts (Lakowski & Hekimi, 1996) and their long lifespan is not further extended by the eat-2 mutation (Lakowski & Hekimi, 1998), suggesting that clk-1 is necessary for eat-2 induced lifespan extension.
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When the researchers then inserted a copy of the normal gene back into clk-1 mutants, these worms lived a normal life-span.
In contrast, in lin-44/Wnt and egl-20/Wnt mutants, elt-3 expression is also increased, but worms live ~30% and ~25% shorter than their wild-type controls.
In mom-2/Wnt and cwn-2/Wnt mutants, elt-3 expression is increased (a biomarker of young age) and worms live ~35% and ~18% longer compared to wild-type controls.
The worms live in clusters of millions and cover acres.
Longevity experiments revealed that the tmem135 (ok1646) mutants lived for a significantly shorter time than wild-type worms, both at 20°C (normal growth conditions) and 15°C (low temperature), while TMEM135::GFP-overexpressing worms lived for a significantly longer time than wild-type worms at 15°C (Fig. 6C and 6D).
Such mutant worms can be bought off the shelf, whereas the ones with just an extra sir2 gene are a special order.
In order to further confirm the role of c30f12.4 in regulating fat homeostasis in living worms, we crossed c30f12.4 mutant worms with hjSi56, which can express GFP-DGAT-2, a marker of lipid droplets (Xu et al., 2012; Klemm et al., 2013).
Mutant worms with reduced insulin signaling (mutation in insulin/insulin like receptor (igf), daf2) live twice as long as wild-type ones [ 186].
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