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| Content Provider | PubMed Central |
|---|---|
| Author | Ayyadevara, Srinivas Tazearslan, Çagdaþ Bharill, Puneet Alla, Ramani Siegel, Eric Reis, Robert J. Shmookler |
| Abstract | Two age-1 nonsense mutants, truncating the class-I phosphatidylinositol 3-kinase catalytic subunit (PI3KCS) before its kinase domain, confer extraordinary longevity and stress-resistance to Caenorhabditis elegans. These traits, unique to second-generation homozygotes, are blunted at the first generation and are largely reversed by additional mutations to DAF-16/FOXO, a transcription factor downstream of AGE-1 in insulin-like signaling. The strong age-1 alleles (mg44, m333) were compared with the weaker hx546 allele on expression microarrays, testing four independent cohorts of each allele. Among 276 genes with significantly differential expression, 92% showed fewer transcripts in adults carrying strong age-1 alleles rather than hx546. This proportion is significantly greater than the slight bias observed when contrasting age-1 alleles to wild-type worms. Thus, transcriptional changes peculiar to nonsense alleles primarily involve either gene silencing or failure of transcriptional activation. A subset of genes responding preferentially to age-1-nonsense alleles was reassessed by real-time polymerase chain reaction, in worms bearing strong or weak age-1 alleles; nearly all of these were significantly more responsive to the age-1(mg44) allele than to age-1(hx546). Additional mutation of daf-16 reverted the majority of altered mg44-F2 expression levels to approximately wild-type values, although a substantial number of genes remained significantly distinct from wild-type, implying that age-1(mg44) modulates transcription through both DAF-16/FOXO-dependent and –independent channels. When age-1-inhibited genes were targeted by RNA interference (RNAi) in wild-type or age-1(hx546) adults, most conferred significant oxidative-stress protection. RNAi constructs targeting two of those genes were shown previously to extend life, and RNAi’s targeting five novel genes were found here to increase lifespan. PI3K-null mutants may thus implicate novel mechanisms of life extension. |
| Related Links | http://dx.doi.org/10.1111/j.1474-9726.2009.00524.x |
| Ending Page | 725 |
| Page Count | 20 |
| Starting Page | 706 |
| File Format | |
| ISSN | 14749718 |
| e-ISSN | 14749726 |
| Journal | Aging cell |
| Issue Number | 6 |
| Volume Number | 8 |
| Language | English |
| Publisher Date | 2009-12-01 |
| Access Restriction | Open |
| Subject Keyword | Cell Biology Ageing Research in Higher Education |
| Content Type | Text |
| Resource Type | Article |
| Subject | Cell Biology Aging |
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