Cell proliferation and differentiation require signalling pathways that enforce appropriate and timely gene expression. We find that Tor2, the catalytic subunit of the TORC1 complex in fission yeast, targets a conserved nuclear RNA elimination network, particularly the serine and proline-rich protein Pir1, to control gene expression through RNA decay and facultative heterochromatin assembly. Phosphorylation by Tor2 protects Pir1 from degradation by the ubiquitin-proteasome system involving the polyubiquitin Ubi4 stress-response protein and the Cul4–Ddb1 E3 ligase. This pathway suppresses widespread and untimely gene expression and is critical for sustaining cell proliferation. Moreover, we find that the dynamic nature of Tor2-mediated control of RNA elimination machinery defines gene expression patterns that coordinate fundamental chromosomal events during gametogenesis, such as meiotic double-strand-break formation and chromosome segregation. These findings have important implications for understanding how the TOR signalling pathway reprogrammes gene expression patterns and contributes to diseases such as cancer.

细胞增殖和分化需要信号通路来强制执行适当和及时的基因表达。我们发现 Tor2 是裂殖酵母中 TORC1 复合物的催化亚基，靶向保守的核 RNA 消除网络，特别是富含丝氨酸和脯氨酸的蛋白质 Pir1，通过 RNA 衰变和兼性异染色质组装来控制基因表达。Tor2 的磷酸化保护 Pir1 免于被涉及多聚泛素 Ubi4 应激反应蛋白和 Cul4–Ddb1 E3 连接酶的泛素-蛋白酶体系统降解。该途径抑制广泛和不合时宜的基因表达，对维持细胞增殖至关重要。而且，我们发现 Tor2 介导的 RNA 消除机制控制的动态特性定义了基因表达模式，这些模式在配子发生过程中协调基本的染色体事件，例如减数分裂双链断裂形成和染色体分离。这些发现对于理解 TOR 信号通路如何重编程基因表达模式并导致癌症等疾病具有重要意义。