Martianov Igor, Viville Stephane, Davidson Irwin
Institut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), CNRS/INSERM/ULP, B.P. 163, 67404 Illkirch Cédex, Communauté Urbaine de Strasbourg, France.
Science. 2002 Nov 1;298(5595):1036-9. doi: 10.1126/science.1076327.
Inactivation of the murine TATA binding protein (TBP) gene by homologous recombination leads to growth arrest and apoptosis at the embryonic blastocyst stage. However, after loss of TBP, RNA polymerase II (pol II) remains in a transcriptionally active phosphorylation state, and in situ run-on experiments showed high levels of pol II transcription comparable to those of wild-type cells. In contrast, pol I and pol III transcription was arrested. Our results show a differential dependency of the RNA polymerases on TBP and provide evidence for TBP-independent pol II transcriptional mechanisms that allow reinitiation and maintenance of gene transcription in vivo.
通过同源重组使小鼠TATA结合蛋白(TBP)基因失活会导致胚胎囊胚阶段的生长停滞和细胞凋亡。然而,TBP缺失后,RNA聚合酶II(pol II)仍处于转录活性磷酸化状态,原位连续转录实验表明,pol II转录水平与野生型细胞相当。相比之下,pol I和pol III转录则被阻断。我们的结果显示了RNA聚合酶对TBP的不同依赖性,并为体内基因转录的重新起始和维持提供了不依赖TBP的pol II转录机制的证据。