Department of Applied Life Science, Sojo University, 4-22-1 Ikeda, Kumamoto City, Japan.
Mech Ageing Dev. 2011 Apr;132(4):210-2. doi: 10.1016/j.mad.2011.02.005. Epub 2011 Feb 25.
The increased lifespan caused by food limitation has been observed in a wide range of animals including the nematode Caenorhabditis elegans. We show here that the lifespans of eat-2 and eat-5 feeding-defective mutants and a mutant of dbl-1 encoding a TGFβ ligand significantly change between the cultures fed on Escherichia coli strain OP50 or a more nutrient-rich strain HB101. On HB101 food, the eat-2, eat-5 and dbl-1 mutants show increased lifespan compared to that of the wild type. This result is probably due to nutrient limitation because the eat mutations reduce food uptake and the mutation of dbl-1 that regulates expression of several digestive enzymes leads to nutrient limitation. In contrast, the lifespans of the eat-2 and dbl-1 mutants decreased from that of the wild type on OP50 food. We found that live OP50 cells within a worm were markedly more in these mutants than in the wild type, which suggests that impaired digestion of pathogenic OP50 decreased lifespan in the eat-2 and dbl-1 mutants.
在包括线虫秀丽隐杆线虫在内的广泛动物中，都观察到了因食物限制而导致的寿命延长。我们在这里表明，在以大肠杆菌 OP50 菌株或更富营养的 HB101 菌株喂养的培养物中，进食缺陷突变体 eat-2 和 eat-5 以及编码 TGFβ 配体的 dbl-1 突变体的寿命会发生显著变化。在 HB101 食物上，与野生型相比，eat-2、eat-5 和 dbl-1 突变体的寿命延长。这一结果可能是由于营养限制造成的，因为 eat 突变会减少食物摄取，而 dbl-1 突变会调节几种消化酶的表达，从而导致营养限制。相比之下，eat-2 和 dbl-1 突变体在 OP50 食物上的寿命比野生型短。我们发现，这些突变体中活的 OP50 细胞明显多于野生型，这表明对致病性 OP50 的消化受损会缩短 eat-2 和 dbl-1 突变体的寿命。
