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Identification of a Novel PP2A Regulator, WNK1, as Critical For Uterine Function

ABSTRACT: Identification of a Novel PP2A Regulator, WNK1, as Critical For Uterine Function

PROVIDER: PRJNA604976 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11027568_1.fastq.gz	Fastqsanger.gz
	SRR11027568_2.fastq.gz	Fastqsanger.gz
	SRR11027569_1.fastq.gz	Fastqsanger.gz
	SRR11027569_2.fastq.gz	Fastqsanger.gz
	SRR11027570_1.fastq.gz	Fastqsanger.gz

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Identification of a Novel PP2A Regulator, WNK1, as Critical For Uterine Function

Project description:We report the transcriptomic profile of uterine tissues obtained from the control (Wnk1f/f) and Wnk1 cKO (PGRCre/+;Wnk1f/f) mice during pseudopregnancy day 4.5.

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Project description:The appropriate development of myeloid progenitors into macrophages, the body’s professional phagocyte, is essential for organismal development, especially in mammals1. This dependence is exemplified by the observation that loss-of-function mutation in colony stimulating factor 1 receptor (CSF1R) results in multiple tissue abnormalities including osteopetrosis2. Despite this importance, little is known about the molecular and cell biological regulation of macrophage development. Here, we report the surprising finding that the chloride-sensing kinase With-no-lysine 1 (WNK1) is required for embryonic development of tissue-resident macrophages (TRMs). Myeloid-specific deletion of Wnk1 caused a dramatic loss of TRMs and subsequently disrupted organ development, induced systemic neutrophilia, and resulted in mortality between 3 and 4 weeks of age. Specifically, we observed that WNK1 absence stalled macrophage differentiation at the myeloid multipotent progenitor (MPP) stage, instead skewing MPP differentiation towards granulopoiesis. Mechanistically, the cognate CSF1R cytokine, macrophage-colony stimulating factor (M-CSF), triggers macropinocytosis in myeloid progenitors, which in turn induces phosphorylation of WNK1. Importantly, macropinocytosis by myeloid progenitors increases cytosolic chloride, which is directly sensed by WNK1. Perturbing chloride flux during macropinocytosis, inhibiting WNK1 chloride-sensing, and blocking macropinocytosis each skew progenitor differentiation from macrophage lineage to granulocyte lineage. Thus, we have uncovered a novel mechanism that links a cell biological process to a molecular circuit whereby WNK1 chloride-sensing and chloride flux act downstream of M-CSF-induced macropinocytosis by multipotent progenitors to ensure macrophage lineage fidelity.

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Transcriptome analysis of rigosertib resistant MDA-MB-453 cells, obtained from a CRISPR screen with WNK1 depletion.

Project description:In a genome-wide CRISPR-Cas9 resistance drug screen, we identified the master osmostress regulator WNK1 kinase as a modulator of the response to the mitotic drug rigosertib. Osmotic stress and WNK1 inactivation lead to an altered response not only to rigosertib but also to other microtubule-related drugs, minimizing the prototypical mitotic arrest produced by these drugs. This effect is due to an alteration in microtubule stability and polymerization dynamics, likely maintained by fluctuations in intracellular molecular crowding upon WNK1 inactivation. This promotes resistance to microtubule depolymerizing drugs, and increased sensitivity to microtubule stabilizing drugs. In summary, our data proposes WNK1 osmoregulation activity as a biomarker for microtubule-associated chemotherapy response.

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Meiotic completion of the spermatocytes requires the kinase WNK1

Project description:The kinase protein WNK1 is highly expressed and phosphorylated in the testis, suggesting possible functions in regulating male fertility. Indeed, conditional pachytene-spermatocyte Wnk1 knock-out mice generated using the novel Wnt7a-Cre failed to produce functional sperm which resulted from the primary spermatogenic arrest during mid-pachynema. Global transcriptomic approaches identified ‘translation’ as one of the impacted events in Wnk1-depleted spermatocytes.

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