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Overexpression of the C.elegans p53 homolog, cep- 1, caused wide-spread cell death independently of caspase activation.
Testing for cep-1 dependent genes in the cep-1 gk138 cep-1 gk138could only confirm 1 of the 28 cep-1 regulalleleandidates even though only one candidate gene wes below detecould levels onlyhe Affymetrix arrays.
Likewise, none of the 87 genes that appeared to be cep-1 lg12501) cep-1 lg12501e reprodependentn the cep-1(gk138) strain.
Around 40% of the CEP-1 activated ncRNAs promoters contain a putative CEP-1-binding site.
(B) Chromosomal distribution of 19 CEP-1 repressed ncRNA clusters.
However, in contrast to the CEP-1 regulated ncRNAs, the CEP-1 regulated mRNAs are not concentrated on chromosome X (Derry et al., 2007).
In C. elegans, CEP-1 is the sole homolog of the p53 family of genes.
Two C. elegans strains, N2 (wild-type) and the cep-1 mutant (gk138), were used.
The majority of the differentially expressed ncRNAs (1014) showed higher expression in the cep-1 mutant (i.e., in the absence of CEP-1) than in the wild-type, and only 16.1% of the ncRNAs (195) showed reduced expression in the cep-1 mutant (Fig. 4A, Tables S6 and S7), suggesting that CEP-1 contributes more to repression than to activation of ncRNA loci.
CEP-1 regulated ncRNAs were frequently clustered and concentrated on the X chromosome.
It is worth mentioning that CEP-1 is highly conserved in prokaryotes and eukaryotes, and human CEP-1 shares 100%% homology of a 9 amino acid span with P. gingivalis α-enolase [37].
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