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Toxoplasma gondii Cyclin-4 Interactome

ABSTRACT: Toxoplasma endodyogeny is governed by a set of Cdk-related kinases (Crk). In this study we investigated TgCrk4 and its cyclin partner TgCyc4. This complex regulates many cell cycle related processes at the G2 phase. To beter undestand the funtion of the TgCrk4/TgCyc4 complex we analyzed the interactome of TgCyc4.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Toxoplasma Gondii Me49

TISSUE(S): Cell Culture

SUBMITTER: Clem Marsilia

LAB HEAD: Elena S. Suvorova

PROVIDER: PXD043994 | Pride | 2024-06-16

REPOSITORIES: pride

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			Action	DRS
	20210202_RH-TIR-HA_control-1.raw	Raw
	20210202_RH-TIR-HA_control-2.raw	Raw
	20230201_LS_cyclin4-IP_a.raw	Raw
	20230201_LS_cyclin4-IP_b.raw	Raw
	mqpar.xml	Xml

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Publications

The Crk4-Cyc4 complex regulates G<sub>2</sub>/M transition in Toxoplasma gondii.

Hawkins Lauren M LM Wang Chengqi C Chaput Dale D Batra Mrinalini M Marsilia Clem C Awshah Danya D Suvorova Elena S ES

The EMBO journal 20240410 11

A versatile division of apicomplexan parasites and a dearth of conserved regulators have hindered the progress of apicomplexan cell cycle studies. While most apicomplexans divide in a multinuclear fashion, Toxoplasma gondii tachyzoites divide in the traditional binary mode. We previously identified five Toxoplasma CDK-related kinases (Crk). Here, we investigated TgCrk4 and its cyclin partner TgCyc4. We demonstrated that TgCrk4 regulates conventional G<sub>2</sub> phase processes, such as repress ...[more]

PMID: 38600241

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2024-06-16 | PXD043924 | Pride

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Project description:Toxoplasma endodyogeny is governed by a set of Cdk-related kinases (Crk). In this study we investigated TgCrk4 and its cyclin partner TgCyc4. This complex regulates many cell cycle related processes at the G2 phase. To beter undestand the funtion of the TgCrk4/TgCyc4 complex we analyzed the interactome of TgCyc4 and TgCrk4 independanlty.

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Project description:The v-Crk protein was originally isolated as the oncogene fusion product of the CT10 chicken retrovirus. Cellular homologues of v-Crk include Crk, which encodes two alternatively spliced proteins (CrkI and CrkII), and CrkL. Though CrkI/II proteins are elevated in several types of cancer, including breast, the question of whether these Crk adaptor proteins can promote breast cancer has not been addressed. We created a transgenic mouse model that allows the expression of CrkII through the hormonally responsive mouse mammary tumor virus promoter. During puberty, transgenic mice were found to have delayed ductal outgrowth, characterized by increased collagen surrounding the terminal end buds. In post-pubertal mice, precocious ductal branching was observed and associated with increased proliferation. Focal mammary tumors appeared in a subset of animals, with a latency of approximately 15 months. Mouse mammary tumor virus/CrkII tumors showed high levels of Crk protein as well as various cytokeratin markers characteristic of their respective tumor pathologies. This study demonstrates that the precise expression of CrkII is critical for integrating signals for ductal outgrowth and branching morphogenesis during mammary gland development. Furthermore, this study provides evidence for a potential role of CrkII in integrating signals for breast cancer progression in vivo, which has important implications for elevated CrkII observed in human cancer.

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