The characterization of zebrafish antimorphic mib alleles reveals that Mib and Mind bomb-2 (Mib2) function redundantly

Zhang, Chengjin; Li, Qing; Lim, Chiaw-Hwee; Qiu, Xuehui; Jiang, Yun-Jin

doi:10.1016/j.ydbio.2007.01.034

Cited by 51 publications

(65 citation statements)

References 82 publications

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“…Previous studies have suggested that whereas DeltaD is a substrate for Mib1, DeltaC, expressed in a small subset of neuronal progenitors (Smithers et al, 2000), is a substrate for both Mib1 and its paralog, Mib2 (Zhang et al, 2007a;Zhang et al, 2007b). Consistent with the specific requirement of Mib1 for DeltaD ubiquitylation, DeltaD is on the cell surface in both mib1 ta52b and mib1 m178 embryos ( Fig.…”

Section: Deltac Endocytosis Is Regulated Differently From Deltad and supporting

confidence: 77%

“…The mib1 m178 allele encodes a truncated Mib1 m178 protein that lacks the third RING domain essential for its ubiquitin ligase function (Itoh et al, 2003). Nonsense-mediated degradation of mib1 m178 transcript significantly reduces the amounts of the mutant protein and its phenotype is like that of a null mutant (Zhang et al, 2007b). By contrast, the mib1 ta52b transcript, which is relatively stable, encodes a Met to Arg substitution in the third RING domain.…”

Section: Discussionmentioning

confidence: 99%

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Interaction with Notch determines endocytosis of specific Delta ligands in zebrafish neural tissue

Matsuda

Chitnis

2009

Development

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Mind bomb1 (Mib1)-mediated endocytosis of the Notch ligand DeltaD is essential for activation of Notch in a neighboring cell. Although most DeltaD is localized in cytoplasmic puncta in zebrafish neural tissue, it is on the plasma membrane in mib1 mutants because Mib1-mediated endocytosis determines the normal subcellular localization of DeltaD. Knockdown of Notch increases cell surface DeltaA and DeltaD, but not DeltaC, suggesting that,like Mib1, Notch regulates endocytosis of specific ligands. Transplant experiments show that the interaction with Notch, both in the same cell (in cis) and in neighboring cells (in trans), regulates DeltaD endocytosis. Whereas DeltaD endocytosis following interaction in trans activates Notch in a neighboring cell, endocytosis of DeltaD and Notch following an interaction in cis is likely to inhibit Notch signaling by making both unavailable at the cell surface. The transplantation experiments reveal a heterogeneous population of progenitors: in some, cis interactions are more important; in others, trans interactions are more important; and in others, both cis and trans interactions are likely to contribute to DeltaD endocytosis. We suggest that this heterogeneity represents the process by which effective lateral inhibition leads to diversification of progenitors into cells that become specialized to deliver or receive Delta signals, where trans and cis interactions with Notch play differential roles in DeltaD endocytosis.

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Section: Deltac Endocytosis Is Regulated Differently From Deltad and supporting

confidence: 77%

Section: Discussionmentioning

confidence: 99%

Interaction with Notch determines endocytosis of specific Delta ligands in zebrafish neural tissue

Matsuda

Chitnis

2009

Development

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“…In mice, RBP-J deletion in FOXD1 cells (mural and renin cell progenitors) causes renal developmental defects and a severe reduction in renin expression (46). The requirement of Notch signaling for ren expression in developing fish was assessed in Notch signalingimpaired mib ta52b mutants, which are phenotypically the strongest of mutant mib alleles (82). The ubiquitin ligase mib is essential for the Delta-mediated activation of the transmembrane Notch receptor in target cells (29).…”

Section: Notch Signaling and Renin Expression Mammalian Renin Cells mentioning

confidence: 99%

Renin expression in developing zebrafish is associated with angiogenesis and requires the Notch pathway and endothelium

Rider

Mullins

Verdon

et al. 2015

American Journal of Physiology-Renal Physiology

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Rider SA, Mullins LJ, Verdon RF, MacRae CA, Mullins JJ. Renin expression in developing zebrafish is associated with angiogenesis and requires the Notch pathway and endothelium. Am J Physiol Renal Physiol 309: F531-F539, 2015. First published July 22, 2015 doi:10.1152/ajprenal.00247.2015.-Although renin is a critical regulatory enzyme of the cardiovascular system, its roles in organogenesis and the establishment of cardiovascular homeostasis remain unclear. Mammalian renin-expressing cells are widespread in embryonic kidneys but are highly restricted, specialized endocrine cells in adults. With a functional pronephros, embryonic zebrafish are ideal for delineating the developmental functions of renin-expressing cells and the mechanisms governing renin transcription. Larval zebrafish renin expression originates in the mural cells of the juxtaglomerular anterior mesenteric artery and subsequently at extrarenal sites. The role of renin was determined by assessing responses to renin-angiotensin system blockade, salinity variation, and renal perfusion ablation. Renin expression did not respond to renal flow ablation but was modulated by inhibition of angiotensin-converting enzyme and altered salinity. Our data in larval fish are consistent with conservation of renin's physiological functions. Using transgenic renin reporter fish, with mindbomb and cloche mutants, we show that Notch signaling and the endothelium are essential for developmental renin expression. After inhibition of angiogenesis, renin-expressing cells precede angiogenic sprouts. Arising from separate lineages, but relying on mutual interplay with endothelial cells, renin-expressing cells are among the earliest mural cells observed in larval fish, performing both endocrine and paracrine functions. renin; zebrafish; notch; endothelium; angiogenesis RENIN is the rate-limiting enzyme of the renin-angiotensin system (RAS). Mammalian ANG II, the effector of the RAS, is principally involved in blood pressure homeostasis by regulation of vasomotor tone and Na ϩ retention. ANG II also regulates cell proliferation and angiogenesis (12,22). Pathological activation of the RAS is associated with cardiovascular diseases, including hypertension and heart failure, and is consequently a major target of therapeutic agents (11).Renin and its cognate cells are required for normal renal development (2), including angiogenesis of the renal vascular tree (59). In mice, ablation of the renin gene or renin-expressing cells leads to renal developmental abnormalities (55,71,79). The vasculature of mammalian embryonic kidneys have a transient but extensive coverage of mural renin-expressing cells (17,31,32,47,63); however, their function is unclear. Adult renin-expressing cells are restricted to the juxtaglomerular apparatus and play a vital role in ion homeostasis by secreting activated renin enzyme via cytoplasmic granules (17,31,36,63). Upon physiological challenge by RAS inhibition or low Na ϩ , prearteriolar vascular smooth muscle cells (VSMC) reestablish their embryonic re...

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“…The treatment induced looped tail and impaired somitogenesis (supplementary material Fig. S3A,B), developmental defects that result from reduced Notch signalling (Zhang et al, 2007). Expression of the Notch target her6 and her15 was also reduced (supplementary material Fig.…”

Section: Notch Signalling Inhibition Reduces Proliferation and Impairmentioning

confidence: 99%

Notch regulates blastema proliferation and prevents differentiation during adult zebrafish fin regeneration

2013

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SUMMARYZebrafish have the capacity to regenerate several organs, including the heart and fins. Fin regeneration is epimorphic, involving the formation at the amputation plane of a mass of undifferentiated, proliferating mesenchymal progenitor-like cells, called blastema. This tissue provides all the cell types that form the fin, so that after damage or amputation the fin pattern and structure are fully restored. How blastema cells remain in this progenitor-like state is poorly understood. Here, we show that the Notch pathway plays an essential role during fin regeneration. Notch signalling is activated during blastema formation and remains active throughout the regeneration process. Chemical inhibition or morpholino-mediated knockdown of Notch signalling impairs fin regeneration via decreased proliferation accompanied by reduced expression of Notch target genes in the blastema. Conversely, overexpression of a constitutively active form of the Notch1 receptor (N1ICD) in the regenerating fin leads to increased proliferation and to the expansion of the blastema cell markers msxe and msxb, as well as increased expression of the proliferation regulator aldh1a2. This blastema expansion prevents regenerative fin outgrowth, as indicated by the reduction in differentiating osteoblasts and the inhibition of bone regeneration. We conclude that Notch signalling maintains blastema cells in a plastic, undifferentiated and proliferative state, an essential requirement for fin regeneration.

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The characterization of zebrafish antimorphic mib alleles reveals that Mib and Mind bomb-2 (Mib2) function redundantly

Cited by 51 publications

References 82 publications

Interaction with Notch determines endocytosis of specific Delta ligands in zebrafish neural tissue

Interaction with Notch determines endocytosis of specific Delta ligands in zebrafish neural tissue

Renin expression in developing zebrafish is associated with angiogenesis and requires the Notch pathway and endothelium

Notch regulates blastema proliferation and prevents differentiation during adult zebrafish fin regeneration

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