Long non-coding RNA INXS is a critical mediator of BCL-XS induced apoptosis.
Bottom Line: These effects were abrogated in the presence of INXS knockdown.Similarly, ectopic INXS overexpression caused a shift in splicing toward BCL-XS and activation of caspases, thus leading to apoptosis.BCL-XS protein accumulation was detected upon INXS overexpression.
Affiliation: Departamento de Bioquímica, Instituto de Química, Universidade de São Paulo, 05508-900 São Paulo, SP, Brasil.Show MeSH
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Mentions: Inspection of the ChIP-seq data from the ENCODE project (42) indicated that the RNA polymerase II (RNAPII) chromatin mark was enriched at the putative transcription start site of INXS within the BCL-X genomic locus. To determine if INXS is transcribed by RNAPII, cells were treated with the RNAPII inhibitor α-amanitin; ∼90% reduction of INXS levels was observed (Figure 3A). In addition, we determined that the INXS lncRNA is modified by a methyl-guanosine cap, using the tobacco acid pyrophosphatase/5′exonuclease assay (Figure 3B). The half-life of INXS was determined to be ∼3 h (Figure 3C). For comparison, the measured half-life of MYC was 29 min, which is comparable with its half-life in the literature (43). Cell fractionation experiments revealed that INXS is predominantly enriched in the nucleus (Figure 3D).
Affiliation: Departamento de Bioquímica, Instituto de Química, Universidade de São Paulo, 05508-900 São Paulo, SP, Brasil.