{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nWDR62 is an essential gene for proper cerebral cortical development. It is highly expressed in neural progenitors during embryonic neurogenesis, and mutations in WDR62 are associated with a wide spectrum of severe brain malformations—including microcephaly, pachygyria, polymicrogyria, and lissencephaly—reflecting its vital role in the regulation of proliferation and migration of neuronal precursors. Loss‐of‐function mutations lead to aberrant neurogenesis and disruption of cortical organization, as demonstrated in both human patients and animal models."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "11"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nAt the cellular level, WDR62 plays a critical role in mitotic regulation by localizing predominantly to the spindle poles, where it fosters proper spindle formation, orientation, and dynamics. It facilitates astral microtubule assembly and coordinates microtubule minus‐end depolymerization by recruiting mitotic effectors such as CEP170, KIF2A, and the microtubule–severing enzyme katanin. Furthermore, its phosphorylation by mitotic kinases like PLK1 ensures correct spindle orientation during symmetric division."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "12", "end_ref": "16"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its role in ensuring proper mitosis, WDR62 functions as a scaffold protein within the c‐Jun N-terminal kinase (JNK) signaling cascade. It directly interacts with and promotes the activation of JNK and its upstream activator MKK7, thereby regulating stress responses and influencing processes such as apoptosis and differentiation. Abnormalities in this pathway—resulting from mutant forms of WDR62—disrupt not only neurogenesis but may also alter cell survival mechanisms."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "17", "end_ref": "21"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn recent studies, aberrant expression of WDR62 has also emerged as a contributor to oncogenesis. Overexpression in various cancers—including lung adenocarcinoma, bladder cancer, colorectal cancer, and metastatic prostate cancer—correlates with more aggressive tumor behavior, centrosome amplification, and chemoresistance. These data highlight an oncogenic function for WDR62 that is, in part, mediated through its interaction with other proteins such as TPX2 and CUL4B, and its promotion of MAPK pathway activities."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "22", "end_ref": "28"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nMoreover, WDR62 is implicated in the initiation of meiosis in female germ cells where it functions as a permissive factor. Its role in retinoic acid–induced STRA8 expression, which is mediated via JNK signaling activation, uncovers yet another facet of its involvement in developmental processes beyond neurogenesis."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "29"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nAdditional clinical and genetic studies further emphasize the heterogeneous and pleiotropic nature of WDR62 mutations. Detailed genotype–phenotype correlations reveal that, while mutations in WDR62 are classically associated with primary microcephaly and cortical malformations, the phenotypic spectrum may extend to include epilepsy with severe neuromotor deficits, as well as rare dermatological abnormalities. These observations, along with findings of co‐occurring mutations and genetic interactions (e.g. with CUL4B), refine our understanding of WDR62’s multifaceted roles in both developmental disorders and cell cycle regulation."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "30", "end_ref": "37"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Kaya Bilgüvar, Ali Kemal Oztürk, Angeliki Louvi, et al. 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