Oncode Institute, Division of Biochemistry, Netherlands Cancer Institute, 1066CX Amsterdam, Netherlands.
Department of Physiology, School of Medicine, University of Patras, 26504 Patras, Greece.
Science. 2022 May 20;376(6595):eabn6020. doi: 10.1126/science.abn6020.
The detyrosination-tyrosination cycle involves the removal and religation of the C-terminal tyrosine of α-tubulin and is implicated in cognitive, cardiac, and mitotic defects. The vasohibin-small vasohibin-binding protein (SVBP) complex underlies much, but not all, detyrosination. We used haploid genetic screens to identify an unannotated protein, microtubule associated tyrosine carboxypeptidase (MATCAP), as a remaining detyrosinating enzyme. X-ray crystallography and cryo-electron microscopy structures established MATCAP's cleaving mechanism, substrate specificity, and microtubule recognition. Paradoxically, whereas abrogation of tyrosine religation is lethal in mice, codeletion of MATCAP and SVBP is not. Although viable, defective detyrosination caused microcephaly, associated with proliferative defects during neurogenesis, and abnormal behavior. Thus, MATCAP is a missing component of the detyrosination-tyrosination cycle, revealing the importance of this modification in brain formation.
去酪氨酸化-酪氨酸化循环涉及α-微管蛋白 C 末端酪氨酸的去除和再连接,与认知、心脏和有丝分裂缺陷有关。血管抑肽-小血管抑肽结合蛋白(SVBP)复合物是许多(但不是全部)去酪氨酸化的基础。我们使用单倍体遗传筛选鉴定了一个未注释的蛋白质,微管相关酪氨酸羧肽酶(MATCAP),作为剩余的去酪氨酸化酶。X 射线晶体学和冷冻电子显微镜结构确立了 MATCAP 的切割机制、底物特异性和微管识别。矛盾的是,尽管酪氨酸再连接的阻断在小鼠中是致命的,但 MATCAP 和 SVBP 的共同缺失并非如此。尽管存活下来,但缺陷的去酪氨酸化导致小头畸形,与神经发生过程中的增殖缺陷有关,并伴有异常行为。因此,MATCAP 是去酪氨酸化-酪氨酸化循环的缺失成分,揭示了这种修饰在大脑形成中的重要性。