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The long and the short of TRF2 in neurogenesis

机译：神经发生中TRF2的长短

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Gene expression patterns change dramatically during neuronal development. Proliferating cells, including neural stem cells (NSCs), express telomere repeat-binding factor 2 (TRF2), a nuclear protein that associates with telomeric proteins, DNA, and RNA telomeres. In NSCs TRF2 also binds to the transcription regulator REST to facilitate repression of numerous neuron-specific genes, thereby keeping the NSCs in a self-renewing state. Upon neuronal differentiation, TRF2 levels decline, REST-regulated neuronal genes are derepressed, and a short isoform of TRF2 arises (TRF2-S) which localizes in the cytoplasm, associates with different subsets of proteins and transcripts, and mobilizes axonal G-rich mRNAs. We recently identified two RNA-binding proteins, HNRNPH1 and H2 (referred to jointly as HNRNPH due to their high homology), which mediate the alternative splicing of an exon required for the expression of full-length TRF2. As HNRNPH levels decline during neurogenesis, TRF2 abundance decreases and TRF2-S accumulates. Here, we discuss the shared and unique functions of TRF2 and TRF2-S, the distinct subcellular compartment in which each isoform resides, the subsets of proteins and nucleic acids with which each interacts, and the functional consequences of these ribonucleoprotein interactions. This paradigm illustrates the dynamic mechanisms through which splicing regulation by factors like HNRNPH enable distinct protein functions as cells adapt to developmental programs such as neurogenesis.
机译：基因表达模式在神经元发育过程中发生巨大变化。包括神经干细胞（NSC）在内的增殖细胞表达端粒重复结合因子2（TRF2），这是一种与端粒蛋白，DNA和RNA端粒相关的核蛋白。在NSC中，TRF2还与转录调节因子REST结合，以促进多种神经元特异性基因的抑制，从而使NSC保持自我更新的状态。在神经元分化后，TRF2水平下降，REST调节的神经元基因被阻遏，并且出现了一个短的TRF2亚型（TRF2-S），其定位于细胞质中，与蛋白质和转录本的不同子集相关，并动员了轴突富含G的mRNA。 。我们最近鉴定了两种RNA结合蛋白HNRNPH1和H2（由于它们的高度同源性，共同称为HNRNPH），它们介导全长TRF2表达所需的外显子的选择性剪接。随着HNRNPH水平在神经发生过程中下降，TRF2丰度下降，TRF2-S积累。在这里，我们讨论了TRF2和TRF2-S的共享和独特功能，每个同种型所驻留的独特的亚细胞区室，每个与之相互作用的蛋白质和核酸的子集，以及这些核糖核蛋白相互作用的功能后果。该范例说明了动态机制，当细胞适应诸如神经发生等发育程序时，诸如HNRNPH等因子的剪接调控可实现独特的蛋白质功能。

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