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Haspin regulates mouse embryonic stem cell developmental potencies through Wnt5a mediated asymmetric cell division

ABSTRACT: To investigate the function of Haspin in the mouse embryonic stem cell, we established Haspin knockout cell lines.

ORGANISM(S): Mus musculus

PROVIDER: GSE220824 | GEO | 2023/08/30

REPOSITORIES: GEO

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Haspin regulates mouse embryonic stem cell developmental potencies through Wnt5a mediated asymmetric cell division

Project description:Haspin regulates mouse embryonic stem cell developmental potencies through Wnt5a mediated asymmetric cell division

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Haspin balances the ratio of asymmetric cell division through Wnt5a and regulates cell fate decisions in mouse embryonic stem cells.

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Distinct roles of Haspin in stem cell division and male gametogenesis

Project description:The atypical protein kinase Haspin phosphorylates Histone H3 at threonine-3 (H3T3ph) during mitosis. H3T3ph creates a docking site for the Chromosomal Passenger Complex at the inner centromere, enabling correction of erratic microtubule-chromosome contacts and preventing chromosome mis-segregation. Surprisingly, Haspin knockout in the mouse does not cause developmental defects, except for testicular anomalies. Therefore, the physiological role of this kinase and the mechanistic significance of H3T3ph are in question. We show here that mouse embryonic stem cells that lack or overexpress Haspin are prone to chromosome misalignment. However, the cell population as a whole maintains the ability to expand and differentiate into multiple lineages. Although not essential for pluripotency, Haspin affects the expression of several testis-specific genes. Furthermore, the H3T3ph mark is detected in under-condensed chromatin domains of haploid spermatids, in cis with lysine/arginine methylation marks. We propose that Haspin controls a compound phospho-methyl switch and regulates testis-specific transcription.

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Targeting HASPIN kinase disrupts SR protein-mediated RNA splicing and synergizes with BCL-2 inhibitor venetoclax in AML

Project description:Acute Myeloid Leukemia (AML) is a blood cancer complicated by acquired drug resistance, disease relapse, and low overall survival rates. Combination therapies using multiple targeted inhibitors can effectively treat AML patients. However, combination treatments are limited by the number of useable targets and our ability to create rational pairings using complimentary molecular mechanisms. Here, we used a human kinase domain-targeted CRISPR screen to identify histone H3 associated protein kinase (HASPIN) as a significant, understudied dependency in AML. HASPIN depletion significantly reduced growth rate, induced a cell cycle arrest, and dysregulated transcription in AML. A proteomics datamining study characterized splicing factors as major HASPIN kinase substrates and highlighted HASPIN’s role as a splicing regulatory kinase. Accordingly, HASPIN depletion strongly dysregulated splicing and inversed aberrant, pro-leukemic splicing programs in AML patients. HASPIN inhibitor CHR-6494 effectively reduced cell viability across AML subtypes while sparing healthy cells. Furthermore, a novel combination therapy consisting of CHR-6494 and BCL-2 inhibitor Venetoclax synergistically reduced AML cell viability and resensitized Venetoclax-resistant AMLs to treatment. Our study presents HASPIN kinase as a novel, therapeutic target for AML, underscores an underappreciated role in splicing regulation, and proposes a viable combination treatment for clinical use.

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