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Strip and Cka negatively regulate JNK signalling during Drosophila spermatogenesis

journal contribution
posted on 2022-03-24, 03:37 authored by John La-MarcaJohn La-Marca, Sarah DiepstratenSarah Diepstraten, Amy HodgeAmy Hodge, Hongyan Wang, Adam HartAdam Hart, Helena RichardsonHelena Richardson, W. Gregory Somers
One fundamental property of a stem cell niche is the exchange of molecular signals between its component cells. Niche models, such as the Drosophila melanogaster testis, have been instrumental in identifying and studying the conserved genetic factors that contribute to niche molecular signalling. Here, we identify jam packed (jam), an allele of Striatin interacting protein (Strip), which is a core member of the highly conserved Striatin-interacting phosphatase and kinase (STRIPAK) complex. In the developing Drosophila testis, Strip cellautonomously regulates the differentiation and morphology of the somatic lineage, and non-cell-autonomously regulates the proliferation and differentiation of the germline lineage. Mechanistically, Strip acts in the somatic lineage with its STRIPAK partner, Connector of kinase to AP-1 (Cka), where they negatively regulate the Jun N-terminal kinase (JNK) signalling pathway. Our study reveals a novel role for Strip/Cka in JNK pathway regulation during spermatogenesis within the developing Drosophila testis.


OzDros is supported by a National Health and Medical Research Council enabling grant (418033). J.E.L.M. was supported by a La Trobe University David Myers scholarship and an Australian Research Council Discovery grant (DP170102549 to H.E.R.). S.T.D. was supported by a La Trobe University Postgraduate Research Scholarship. H.E.R. was supported by a National Health and Medical Research Council fellowship (1020056) and funds from the La Trobe Institute for Molecular Science and La Trobe University. H.W. was supported by the Singapore National Medical Research Council (NMRC/CBRG/0082/2015). W.G.S. was supported by a National Health and Medical Research Council Peter Doherty Australian Biomedical Fellowship (520307). A.H.H. was supported by a National Health and Medical Research Council grant (GNT0606691).


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