The role of gastrulation brain homeobox 2 (gbx2) in the development of the ventral telencephalon in zebrafish embryos

Mycobacterium abscessusis a rapidly growingMycobacteriumcausing a wide spectrum of clinical syndromes. It now is recognized as a pulmonary pathogen to which cystic fibrosis patients have a particular susceptibility. TheM. abscessusrough (R) variant, devoid of cell-surface glycopeptidolipids (GPLs), causes more severe clinical disease than the smooth (S) variant, but the underlying mechanisms of R-variant virulence remain obscure. Exploiting the optical transparency of zebrafish embryos, we observed that the increased virulence of theM. abscessusR variant compared with the S variant correlated with the loss of GPL production. The virulence of the R variant involved the massive production of serpentine cords, absent during S-variant infection, and the cords initiated abscess formation leading to rapid larval death. Cording occurred within the vasculature and was highly pronounced in the central nervous system (CNS). It appears thatM. abscessusis transported to the CNS within macrophages. The release ofM. abscessusfrom apoptotic macrophages initiated the formation of cords that grew too large to be phagocytized by macrophages or neutrophils. This study is a description of the crucial role of cording in the in vivo physiopathology ofM. abscessusinfection and emphasizes cording as a mechanism of immune evasion.

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A study of the role of calcium ions during cytokinesis in cleavage stage zebrafish embryos

10.14711/thesis-b843336 ◽

2004 ◽

Author(s):

Karen Wing-man Lee

Keyword(s):

Calcium Ions ◽

Zebrafish Embryos ◽

Cleavage Stage

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Role of SLC12A10.2, a Na-Cl cotransporter-like protein, in a Cl uptake mechanism in zebrafish (Danio rerio)

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00119.2009 ◽

2009 ◽

Vol 296 (5) ◽

pp. R1650-R1660 ◽

Cited By ~ 81

Author(s):

Yi-Fang Wang ◽

Yung-Che Tseng ◽

Jia-Jiun Yan ◽

Junya Hiroi ◽

Pung-Pung Hwang

Keyword(s):

Specific Inhibitor ◽

In Vivo Model ◽

Zebrafish Embryos ◽

Uptake Mechanism ◽

Ion Regulation ◽

Specific Expression ◽

Net Uptake ◽

First Time

The thiazide-sensitive Na+-Cl− cotransporter (NCC), a member of the SLC12 family, is mainly expressed in the apical membrane of the mammalian distal convoluted tubule (DCT) cells, is responsible for cotransporting Na+ and Cl− from the lumen into DCT cells and plays a major role in the mammalian renal NaCl reabsorption. The NCC has also been reported in fish, but the functional role in fish ion regulation is yet unclear. The present study used zebrafish as an in vivo model to test the hypothesis of whether the NCC plays a role in Na+ and/or Cl− uptake mechanisms. Four NCCs were cloned, and only one of them, zebrafish (z) slc12a10.2 was found to predominately and specifically be expressed in gills. Double in situ hybridization/immunocytochemistry in zebrafish skin/gills demonstrated that the specific expression of zslc12a10.2 mRNA in a novel group of ionocytes differed from those of the previously-reported H+-ATPase-rich (HR) cells and Na+-K+-ATPase-rich (NaR) cells. Gill mRNA expression of zslc12a10.2 was induced by a low-Cl environment that stimulated fish Cl− influx, while a low-Na environment suppressed this expression. Incubation with metolazone, a specific inhibitor of the NCC, impaired both Na+ and Cl− influx in 5-day postfertilization (dpf) zebrafish embryos. Translational knockdown of zslc12a10.2 with a specific morpholino caused significant decreases in both Cl− influx and Cl− content of 5-dpf zebrafish embryos, suggesting that the operation of zNCC-like 2 results in a net uptake of Cl− in zebrafish. On the contrary, zslc12a10.2 morphants showed increased Na+ influx and content that resulted from upregulation of mRNA expressions of Na+-H+ exchanger 3b and carbonic anhydrase 15a in HR cells. These results for the first time provide in vivo molecular physiological evidence for the possible role of the NCC in the Cl− uptake mechanism in zebrafish skin/gills.

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Conditional Loss of BAF (mSWI/SNF) Scaffolding Subunits Affects Specification and Proliferation of Oligodendrocyte Precursors in Developing Mouse Forebrain

Frontiers in Cell and Developmental Biology ◽

10.3389/fcell.2021.619538 ◽

2021 ◽

Vol 9 ◽

Author(s):

Eman Abbas ◽

Mohamed A. Hassan ◽

Godwin Sokpor ◽

Kamila Kiszka ◽

Linh Pham ◽

...

Keyword(s):

Chromatin Remodeling ◽

Neural Development ◽

Conditional Knockout ◽

Baf Complex ◽

Ventral Telencephalon ◽

Mouse Mutants ◽

Oligodendrocyte Precursor ◽

Brain And Spinal Cord ◽

The Brain

Oligodendrocytes are responsible for axon myelination in the brain and spinal cord. Generation of oligodendrocytes entails highly regulated multistage neurodevelopmental events, including proliferation, differentiation and maturation. The chromatin remodeling BAF (mSWI/SNF) complex is a notable regulator of neural development. In our previous studies, we determined the indispensability of the BAF complex scaffolding subunits BAF155 and BAF170 for neurogenesis, whereas their role in gliogenesis is unknown. Here, we show that the expression of BAF155 and BAF170 is essential for the genesis of oligodendrocytes during brain development. We report that the ablation of BAF155 and BAF170 in the dorsal telencephalic (dTel) neural progenitors or in oligodendrocyte-producing progenitors in the ventral telencephalon (vTel) in double-conditional knockout (dcKO) mouse mutants, perturbed the process of oligodendrogenesis. Molecular marker and cell cycle analyses revealed impairment of oligodendrocyte precursor specification and proliferation, as well as overt depletion of oligodendrocytes pool in dcKO mutants. Our findings unveil a central role of BAF155 and BAF170 in oligodendrogenesis, and thus substantiate the involvement of the BAF complex in the production of oligodendrocytes in the forebrain.

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A novel role of PRL in regulating epithelial cell density by inducing apoptosis at confluence

Journal of Cell Science ◽

10.1242/jcs.258550 ◽

2021 ◽

Author(s):

Sweksha Lohani ◽

Yosuke Funato ◽

Yuki Akieda ◽

Kiyohito Mizutani ◽

Yoshimi Takai ◽

...

Keyword(s):

Epithelial Cell ◽

Cell Density ◽

Mdck Cells ◽

Zebrafish Embryos ◽

Developmental Defect ◽

Convergent Extension ◽

Regenerating Liver ◽

Phosphatase Of Regenerating Liver ◽

Multicellular Organisms

Maintaining proper epithelial cell density is essential for the survival of multicellular organisms. While regulation of cell density through apoptosis is well known, its mechanistic details remain elusive. Here, we report the involvement of membrane-anchored phosphatase of regenerating liver (PRL), originally known for its role in cancer malignancy, in this process. In epithelial MDCK cells, upon confluence, doxycycline-induced expression of PRL upregulated apoptosis, reducing the cell density. This could be circumvented by artificially reducing the cell density via stretching the cell-seeded silicon chamber. Moreover, siRNA-mediated knockdown of endogenous PRL blocked apoptosis, leading to greater cell density. Mechanistically, PRL promoted apoptosis by upregulating the translation of E-cadherin and activating TGF-β pathway. Morpholino-mediated inhibition of PRL expression in zebrafish embryos caused developmental defect with reduced apoptosis and increased epithelial cell density during convergent extension. This study revealed a novel role of PRL in regulating density-dependent apoptosis in vertebrate epithelium.

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