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Stage-specific degradation of cyclin D3 orchestrates myelopoiesis and restrains MPN development [scRNA-seq]

ABSTRACT: Cyclin D3 is critical for myelopoiesis, with its rapid, stage-specific degradation regulating normal granulocyte-monocyte differentiation. Using a knock-in mouse model with a degradation-resistant cyclin D3 variant (D3T283A), we show that sustained cyclin D3 levels enhance granulocyte-monocyte output, cause microcytic erythrocytes, thrombocytosis, and extramedullary hematopoiesis. Splenic HSPCs from D3T283A mice exhibit increased self-renewal and competitive repopulation advantage. Prolonged D3T283A expression drives a high-penetrance myeloproliferative neoplasm, reducing survival.

ORGANISM(S): Mus musculus

PROVIDER: GSE296132 | GEO | 2026/05/01

REPOSITORIES: GEO

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Stage-specific degradation of cyclin D3 orchestrates myelopoiesis and restrains MPN development [RNA-seq]

Project description:Cyclin D3 is critical for myelopoiesis, with its rapid, stage-specific degradation regulating normal granulocyte-monocyte differentiation. Using a knock-in mouse model with a degradation-resistant cyclin D3 variant (D3T283A), we show that sustained cyclin D3 levels enhance granulocyte-monocyte output, cause microcytic erythrocytes, thrombocytosis, and extramedullary hematopoiesis. Splenic HSPCs from D3T283A mice exhibit increased self-renewal and competitive repopulation advantage. Prolonged D3T283A expression drives a high-penetrance myeloproliferative neoplasm, reducing survival.

2026-05-01 | GSE296131 | GEO

Stage-specific degradation of cyclin D3 orchestrates myelopoiesis and restrains MPN development [RNA-seq]

Project description:Stage-specific degradation of cyclin D3 orchestrates myelopoiesis and restrains MPN development [RNA-seq]

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Stage-specific degradation of cyclin D3 orchestrates myelopoiesis and restrains MPN development [scRNA-seq]

Project description:Stage-specific degradation of cyclin D3 orchestrates myelopoiesis and restrains MPN development [scRNA-seq]

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Project description:Pre-B and pre-T lymphocytes must orchestrate a transition from a highly proliferative state to a quiescent one during development. Cyclin D3 is essential for these cells’ proliferation, but little is known about its post-translational regulation at this stage. Here, we show that the dual specificity tyrosine-regulated kinase 1A (DYRK1A) restrains Cyclin D3 protein levels by phosphorylating T283 to induce its degradation. Loss of DYRK1A activity, via genetic inactivation or pharmacologic inhibition, caused accumulation of Cyclin D3 protein, incomplete repression of E2F-mediated gene transcription, and failure to properly couple cell cycle exit with differentiation. Expression of a non-phosphorylatable Cyclin D3 T283A mutant recapitulated these defects, while inhibition of Cyclin D:CDK4/6 mitigated the effects of DYRK1A inhibition. These data uncover a previously unknown role for DYRK1A in lymphopoiesis, and demonstrate how Cyclin D3 protein stability is negatively regulated during exit from the proliferative phases of B and T cell development.

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