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Bmp5 stimulates Oclna expression to maintain periodic neuromast deposition through PI3K/Akt signaling during zebrafish posterior lateral line development

ABSTRACT: The posterior lateral line (pLL), a mechanosensory organ of fish and amphibians for detecting water flow, develops through caudal migration of the pLL primordium along the horizontal myoseptum and its periodic deposition of neuromasts. Despite that signaling pathways which underlies the regional organization and directional migration of zebrafish pLL primordium have been widely studied, the mechanisms controlling neuromast deposition remain largely unclarified. Here, we uncover that a role of Bmp5-in the regulation of neuromast deposition during pLL development. Loss of bmp5 results in a delay in neuromast deposition, generating a reduced number of more widely spaced neuromasts in pLL without affecting the patterning and migration of primordium. Combining single-cell sequencing and crispant analysis, we further show that the defects in neuromast deposition caused by bmp5 loss of function is closely related to the downregulation of the tight junction protein Occludin a (Oclna) in the trailing proneuromast. Moreover, we have identified PI3K/Akt signaling as a Bmp5 downstream pathway regulating neuromast deposition. Taken together, our study reveals that Bmp5 stimulates Oclna expression to maintain timely deposition of neuromasts by activating PI3K/Akt signaling during zebrafish pLL development.

ORGANISM(S): Danio rerio

PROVIDER: GSE328277 | GEO | 2026/09/30

REPOSITORIES: GEO

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Project description:Hyperactivation of the PI3K/AKT pathway is observed in most NSCLCs, promoting proliferation, migration and resistance to therapy. AKT can be activated through several mechanisms that include loss of the negative regulator PTEN, activating mutations of the catalytic subunit of the positive regulator phosphatydil-inositol-3â phosphate kinase (PIK3CA) and/or mutations of AKT1 itself. However, whereas the effects of AKT activation on mRNAs and proteins in the cell are fairly clear, the role of miRNAs as downstream targets of activated PI3K/AKT signalling is still poorly defined so far. To identify miRNAs that are targets of constitutive signalling of PI3K/AKT in lung cancer cells, we performed miRNA profiling of human lung epithelial cells expressing active mutant AKT1 (E17K), active mutant PI3KCA (E545K) or that are silenced for PTEN. We identified 28 differentially expressed miRNAs (8 up-regulated, 20 down-regulated) that were common to BEAS-AKT1-E17K, BEAS-PIK3CA-E545K and BEAS-shPTEN cells. Among the 8 up-regulated miRNAs that were common to all the alterations, the miRNA most consistently up-regulated by activation of the PI3K/AKT pathway in BEAS-2B cells was miR-196a. The results reported here demonstrate that miR-196a acts as oncogene downstream the PI3K/AKT pathway, mediating the proliferative, pro-migratory and tumorigenic activity of this pathway in NSCLC cells by targeting FoxO1 and p27 expression. By adoptive expression of miR-196a in BEAS-2B cells, we demonstrated that miR-196a stimulates anchorage-dependent and -independent proliferation, migration and tumorigenicity in BEAS-2B cells. On the other hand, by use of antimir-196a in NCI-H460 cells to silence the endogenous expression of miR-196a, we demonstrate that miR-196a plays a pivotal role in mediating the stimulation of proliferation, migration and tumorigenicity induced by aberrant activation of PI3K/AKT signalling. Accordingly, we found that miR-196a was significantly overexpressed in human NSCLC-derived cell lines (n=6) and primary lung cancer samples (n=28). Finally, based on predicted binding sites for miR-196a by microRNA analysis software, we found that miR-196a affects protein levels of FoxO1 and p27 in NSCLC cells.

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Bmp5 stimulates Oclna expression to maintain periodic neuromast deposition through PI3K/Akt signaling during zebrafish posterior lateral line development

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