Poly(A)-binding protein (Pab1 in yeast) is involved in mRNA decay and translation initiation, but its molecular functions are incompletely understood. We found that auxin-induced degradation of Pab1 reduced bulk mRNA and polysome abundance in a manner suppressed by deleting the catalytic subunit of decapping enzyme (dcp2Δ), demonstrating that enhanced decapping/degradation is the major driver of reduced mRNA abundance and protein synthesis at limiting Pab1 levels. An increased median poly(A) tail length conferred by Pab1 depletion was also nullified by dcp2Δ, suggesting that mRNA isoforms with shorter tails are preferentially decapped/degraded at limiting Pab1. In contrast to findings on mammalian cells, the translational efficiencies (TEs) of many mRNAs were altered by Pab1 depletion; however, these changes were broadly diminished by dcp2Δ, suggesting that reduced mRNA abundance is a major driver of translational reprogramming at limiting Pab1. Thus, assembly of the closed-loop mRNP via PABP-eIF4G interaction appears to be dispensable for normal translation of most yeast mRNAs in vivo. Interestingly, histone mRNAs and proteins are preferentially diminished on Pab1 depletion dependent on Dcp2, accompanied by activation of internal cryptic promoters in the manner expected for reduced nucleosome occupancies, revealing a new layer of post-transcriptional control of histone gene expression.

中文翻译：

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酵母多聚 (A) 结合蛋白 (Pab1) 主要通过阻断 mRNA 脱帽和衰变来控制体内翻译起始

Poly(A) 结合蛋白（酵母中的 Pab1）参与 mRNA 降解和翻译起始，但其分子功能尚不完全清楚。我们发现，生长素诱导的 Pab1 降解以通过删除脱帽酶 (dcp2Δ) 的催化亚基来抑制的方式减少了大量 mRNA 和多核糖体丰度，证明增强的脱帽/降解是限制下 mRNA 丰度和蛋白质合成减少的主要驱动因素。 Pab1 水平。 Pab1 耗尽所带来的中位聚 (A) 尾长度的增加也被 dcp2Δ 抵消，这表明尾部较短的 mRNA 亚型在限制 Pab1 时优先脱帽/降解。与哺乳动物细胞的研究结果相反，许多 mRNA 的翻译效率 (TE) 因 Pab1 缺失而改变。然而，这些变化被 dcp2Δ 广泛削弱，这表明 mRNA 丰度的减少是限制 Pab1 的翻译重编程的主要驱动因素。因此，通过 PABP-eIF4G 相互作用组装闭环 mRNA 对于大多数酵母 mRNA 的体内正常翻译似乎是可有可无的。有趣的是，组蛋白 mRNA 和蛋白质在依赖于 Dcp2 的 Pab1 耗尽时优先减少，同时伴随着内部隐性启动子以减少核小体占用的方式激活，揭示了组蛋白基因表达的新的转录后控制层。