Perez-Jimenez, Mercedes M. , RODRIGUEZ PALERO, MARÍA JESÚS, Rodenas, Eduardo , Askjaer, Peter , Munoz, Manuel J.
No
Biogerontology
Article
Científica
2
1
3.29
1.121
01/06/2014
000336029500007
Nuclear envelope (NE) architecture and aging have been associated since the discovery that certain human progeria diseases are due to perturbations in processing of lamin A protein, generating alterations in NE morphology. However, whether changes in the NE are a causal effect of normal and premature aging is still controversial. Caenorhabditis elegans is a model organism where observations supporting both, dependent and independent roles of nuclear architecture in the aging process, have been reported. We found that the long-lived glp-1 mutant and dietary restriction delayed age-associated nuclear morphology changes. In addition, we observed that the long-lived mutant of the insulin/IGF receptor daf-2 delayed the age-dependent changes of nuclear architecture at 25 A degrees C, as previously described. However, when daf-2 animals were incubated at 20 A degrees C they remained long-lived, but nuclear appearance changed at similar rate as in the wild type. This supports the idea that both phenotypes, longevity and maintenance of nuclear architecture are tightly associated but can be separated and argues that nuclear morphology deterioration is not a cause of the natural aging process.
Aging; Dietary restriction; daf-2; IGF/insulin receptor; Nuclear lamina; Progeria