Posttranslational modification of microtubules by the MATCAP detyrosinase.
Lisa LandskronJitske BakAthanassios AdamopoulosKonstantina KaplaniMaria MoraitiLisa G van den HengelJi-Ying SongOnno B BleijerveldJoppe NieuwenhuisTatjana HeidebrechtLinda HennemanMarie Jo MoutinMarin BarisicStavros TaravirasAnastassis PerrakisThijn R BrummelkampPublished in: Science (New York, N.Y.) (2022)
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.
Keyphrases
- electron microscopy
- binding protein
- high resolution
- genome wide
- zika virus
- cerebral ischemia
- intellectual disability
- high throughput
- left ventricular
- white matter
- amino acid
- resting state
- cell cycle
- multiple sclerosis
- heart failure
- magnetic resonance
- autism spectrum disorder
- metabolic syndrome
- functional connectivity
- magnetic resonance imaging
- copy number
- computed tomography
- blood brain barrier
- brain injury
- subarachnoid hemorrhage
- embryonic stem cells
- wild type