The transcription factor NF-Y is a trimer with histone-likesubunits that binds and activates CCAAT-containingpromoters. NF-Y controls the expressionof several key regulators of the cell cycle. In thisstudy, we examined the functional and moleculareffects of NF-YB knockdown. Cell cycle progressionis affected with a G2/M-specific depletion. This isdue to the inability of activation of G2/M-specificgenes, as evidenced by expression profiling, RT-PCRand ChIP data. Surprisingly, apoptosis is alsoobserved, with Caspase 3/7/8 cleavage. A role ofp53 and Bcl-2 family members is important. NF-YBinactivation is sufficient to functionally activate p53,in the absence of DNA damage. Failure to maintain aphysiologic level of CCAAT-dependent transcriptionof anti-apoptotic genes contributes to impairment ofBax/Bcl-2 and Bax/Bcl-XL ratios. Our data highlightthe importance of fine balancing the NF-Y-p53 duofor cell survival by (i) maintaining transcription ofanti-apoptotic genes and (ii) preventing p53 activationthat triggers the apoptotic cascade.

A balance between NF-Y and p53 governs the pro- and anti-apoptotic transcriptional response / Benatti, Paolo; Basile, Valentina; Merico, D; Fantoni, Luca Isaia; Tagliafico, Enrico; Imbriano, Carol. - In: NUCLEIC ACIDS RESEARCH. - ISSN 0305-1048. - STAMPA. - 36 (5)(2008), pp. 1415-1428. [10.1093/nar/gkm1046]

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