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Ret and substrate-derived TGFb maverick regulate space-filling dendrite growth in Drosophila sensory neurons

ABSTRACT: Ret and substrate-derived TGFb maverick regulate space-filling dendrite growth in Drosophila sensory neurons

PROVIDER: PRJNA475213 | ENA |

REPOSITORIES: ENA

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Ret and substrate-derived TGFb maverick regulate space-filling dendrite growth in Drosophila sensory neurons

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Ret and Substrate-Derived TGF-β Maverick Regulate Space-Filling Dendrite Growth in Drosophila Sensory Neurons.

Project description:Dendrite morphogenesis is a highly regulated process that gives rise to stereotyped receptive fields, which are required for proper neuronal connectivity and function. Specific classes of neurons, including Drosophila class IV dendritic arborization (C4da) neurons, also feature complete space-filling growth of dendrites. In this system, we have identified the substrate-derived TGF-β ligand maverick (mav) as a developmental signal promoting space-filling growth through the neuronal Ret receptor. Both are necessary for radial spreading of C4da neuron dendrites, and Ret is required for neuronal uptake of Mav. Moreover, local changes in Mav levels result in directed dendritic growth toward regions with higher ligand availability. Our results suggest that Mav acts as a substrate-derived secreted signal promoting dendrite growth within not-yet-covered areas of the receptive field to ensure space-filling dendritic growth.

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The ELAV/Hu protein Found in neurons regulates cytoskeletal and ECM adhesion inputs for space-filling dendrite growth

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Project description:Drosophila melanogaster Ret, Ret oncogene, is differentially expressed in 13 experiment(s);

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Project description:Drosophila melanogaster Ret, Ret oncogene, is expressed in 3 baseline experiment(s);

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RNA-seq of RET-aberrant cancer cell lines treated with RET-TKI selpercatinib

Project description:RET-aberrant cancer discovered as a relevant targetable oncogene in several types of tumors, whose inhibitors have marked efficacy. However, some of patients with RET-aberrant cancer are insensitive to RET- tyrosine kinase inhibitors (TKIs) and are clinically non-responders. Recently, drug-tolerant mechanisms have been gaining attention as targets for initial therapies aimed at overcoming drug resistance. However, the underlying mechanisms of drug-tolerant cells emergence treated with RET-TKIs derived from RET-aberrant cancer cells remains unknown. In this study, HER3 signal activity through YAP1 was led to maintaining cell survival and inducing the emergence of cells tolerant to RET-TKIs selpercatinib and pralsetinib in high YAP1 expressed RET- rearranged cancer cells. These results suggested that YAP1-HER3 axis plays pivotal roles for cell survival under an exposure with RET-TKIs in the intrinsic resistance to RET-TKIs and the emergence of tolerant cells by RET-TKIs in YAP1 expressed RET-aberrant cancer, suggesting that YAP1/HER3 inhibition and RET-TKIs is a highly potent combination for initial treatment.

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Glia detect and transiently protect against dendrite substructure disruption

Project description:Glia assess axon structure to modulate myelination and axon repair. Whether glia similarly detect dendrites and their substructures is not well understood. Here, we show that glia monitor the integrity of dendrite substructures and transiently protect their perturbation. We demonstrate that disruption of C. elegans sensory neuron dendrite cilia elicits acute glial responses, including increased accumulation of glia-derived extracellular matrix around cilia, changes in gene expression, and alteration of secreted protein repertoire. DGS-1, a 7-transmembrane domain neuronal protein, and FIG-1, a multifunctional thrombospondin-domain glial protein, are required for glial detection of cilia integrity, physically interact, and exhibit mutually-dependent localization to and around cilia, respectively. Glial responses to dendrite cilia disruption transiently protect against damage. Thus, our studies uncover a homeostatic, protective, dendrite glia signaling interaction regulating dendrite substructure integrity.

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RET fusion genes, BCR-RET and FGFR1OP-RET, are associated with chronic myelomonocytic leukemia, display sensitivity to Sorafenib, an inhibitor of tyrosine-kinase activity and enhance monocytic differentiation

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