{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nShugoshin‐1 (SGO1) is a pivotal guardian of sister chromatid cohesion during both mitosis and meiosis. It acts principally to protect centromeric cohesin from premature phosphorylation and removal, thereby ensuring accurate chromosome segregation. SGO1 achieves this by recruiting and interacting with protein phosphatase 2A (PP2A) to counteract cohesin‐destabilizing kinases, and its function is regulated via phosphorylation‐dependent mechanisms involving Bub1‐mediated histone H2A modifications. Furthermore, timely degradation of SGO1 via the anaphase‐promoting complex (APC/C) is essential for the transition from metaphase to anaphase, underscoring its critical role in cell cycle progression."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "7"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its central role in cohesion protection, SGO1 orchestrates proper kinetochore–microtubule attachments and tension sensing. Its activities are fine‐tuned by multiple kinases – including Aurora B, Polo‐like kinase 1 (Plk1), and NEK2A – which phosphorylate SGO1 to modulate its localization between inner centromeres and kinetochores. Alternative splice forms of SGO1 further specialize its function, with certain isoforms localizing to centrosomes to secure centriole cohesion. In addition, chromatin remodelers (for example, RSF1 via HDAC1 recruitment) and the SET oncoprotein regulate the SGO1–cohesin interaction, thereby controlling the timely release of cohesion at anaphase."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "8", "end_ref": "15"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nDysregulation of SGO1 has been implicated in a spectrum of disease states, including various cancers and congenital syndromes. Aberrant expression, mutation, and alternative splicing of SGO1 (or its gene SGOL1) have been linked to chromosome missegregation, aneuploidy, and consequent tumor progression in colorectal, lung, gastric, and renal cancers. Moreover, dominant-negative peptides and altered interactions with regulatory proteins such as CIP2A or long noncoding RNAs further highlight its role in oncogenesis and multidrug resistance. Notably, a deleterious missense mutation in SGO1 (K23E) underlies Chronic Atrial and Intestinal Dysrhythmia (CAID) syndrome by impairing its interaction with key ion-channel regulators (e.g. HCN4), thereby perturbing cardiac pacemaking. Collectively, these studies emphasize that both canonical and noncanonical functions of SGO1 – from safeguarding centromeric integrity and modulating kinetochore attachments to participating in tissue‐specific processes – are critical for maintaining genomic stability and proper cellular function."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "16", "end_ref": "33"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Zhanyun Tang, Yuxiao Sun, Sara E Harley, et al. 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