| Gene name: | BCL6 |
| Aging type: | Accelerate |
| Aging characteristic: |
| Tissue type: | -- |
| Cell name: | WI-38,MEF |
| Experiment: | SA-β-gal activity assay//Flow cytometry//Cell proliferation assay |
| Description: | Consistent with the ability of p53 to induce a G1 arrest, BCL6-transduced WI-38 cells exhibited an increase in the G1 phase fraction from 74 versus 42% in control cells; and a progressive reduction in their proliferative rate that could not be overcome by increasing serum concentration or passage in culture (data not shown).Also, certain morphological features, such as cytoplasmic vacuoles and enlarged cell size and flattening were observed. These changes were suggestive of cellular senescence, which was further confirmed by detection of pH-dependent -galactosidase levels. Altogether,within 8 days, 37.5% of BCL6-transduced WI-38 cells displayed evidence of senescence as compared with 6% of GFP transduced or untransduced cells. |
| Regulatory pathway: | P53 |
| R-AG-Pathway: | Upregulation |
| Official symbol(s): | TP53 |
| Pathway experiment: | Knockdown//Western blot//SA-β-gal activity assay//Proliferation assay |
| Pathway description: | Transduction of BCL6 in Tp53-/- MEFs failed to provoke growth arrest. Senescence was largely p53-dependent because no more than 10% of Tp53- /- MEFs became positive for β-galactosidase. Like WI-38 cells, Tp53+/+ MEFs displayed upregulation of Tp53 upon transduction of BCL6. Not only did BCL6-transduced Tp53 -/- MEFs maintain their proliferative potential, but also acquired the ability to form colonies on tissue culture plates in contrast to control transduced cells. |
Annotation:
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