scholarly journals SNAP to attention: A SNARE complex regulates neuronal progenitor polarity

2020 ◽  
Vol 220 (1) ◽  
Author(s):  
Victor Tarabykin

SNARE vesicle targeting complex controls the polarity of neuronal progenitors. Kunii et al. (2020. J. Cell Biol. https://doi.org/10.1083/jcb.201910080) show that the SNAP23–VAMP8–Syntaxin1B complex is required for membrane targeting of N-cadherin and formation of adherence junction complexes in radial glia neuronal progenitors, the major prerequisite of cell polarity establishment.

2021 ◽  
Author(s):  
Debosree Pal ◽  
Sangeeta Dutta ◽  
Dhanur P Iyer ◽  
Utsa Bhaduri ◽  
Satyanarayana Manchanahalli Rangasw Rao

LncRNA Mrhlhas been shown to be involved in regulating meiotic commitment of mouse spermatogonial progenitors and coordinating differentiation events in mouse embryonic stem cells. Here we have characterized the interplay of Mrhlwith lineage-specific transcription factors during mouse neuronal lineage development. Our results demonstrate that Mrhl is predominantly expressed in the neuronal progenitor populations in mouse embryonic brains and in retinoic acid derived radial-glia like neuronal progenitor cells. Mrhl levels are significantly down regulated in postnatal brains and in maturing neurons. In neuronal progenitors, a master transcription factor, PAX6, acts to regulate the expression of Mrhl through direct physical binding at a major site in the distal promoter, located at 2.9kb usptream of the TSS of Mrhl. Furthermore, NFAT4 occupies the Mrhl proximal promoter at two sites, at 437bp and 143bp upstream of the TSS. ChIP studies reveal that PAX6 and NFAT4 interact with each other, suggesting co-regulation of lncRNA Mrhl expression in neuronal progenitors. Our studies herewith are crucial towards understanding how lncRNAs are regulated by major lineage-specific TFstowardsdefining specific development and differentiation events.


2003 ◽  
Vol 14 (12) ◽  
pp. 4958-4970 ◽  
Author(s):  
Keith G. Kozminski ◽  
Laure Beven ◽  
Elizabeth Angerman ◽  
Amy Hin Yan Tong ◽  
Charles Boone ◽  
...  

Polarized cell growth requires the coupling of a defined spatial site on the cell cortex to the apparatus that directs the establishment of cell polarity. In the budding yeast Saccharomyces cerevisiae, the Ras-family GTPase Rsr1p/Bud1p and its regulators select the proper site for bud emergence on the cell cortex. The Rho-family GTPase Cdc42p and its associated proteins then establish an axis of polarized growth by triggering an asymmetric organization of the actin cytoskeleton and secretory apparatus at the selected bud site. We explored whether a direct linkage exists between the Rsr1p/Bud1p and Cdc42p GTPases. Here we show specific genetic interactions between RSR1/BUD1 and particular cdc42 mutants defective in polarity establishment. We also show that Cdc42p coimmunoprecipitated with Rsr1p/Bud1p from yeast extracts. In vitro studies indicated a direct interaction between Rsr1p/Bud1p and Cdc42p, which was enhanced by Cdc24p, a guanine nucleotide exchange factor for Cdc42p. Our findings suggest that Cdc42p interacts directly with Rsr1p/Bud1p in vivo, providing a novel mechanism by which direct contact between a Ras-family GTPase and a Rho-family GTPase links the selection of a growth site to polarity establishment.


2018 ◽  
Vol 217 (11) ◽  
pp. 3772-3773 ◽  
Author(s):  
Kia Z. Perez-Vale ◽  
Mark Peifer

Cell polarity is regulated by protein networks in the apical and basolateral domains that repress one another by mutually antagonistic interactions. Gamblin et al. (2018. J. Cell Biol. https://doi.org/10.1083/jcb.201803099) reveal that apical Crumbs is antagonized by oligomerization of basolateral Yurt, while Yurt oligomerization is in turn negatively regulated by the apical kinase aPKC.


2014 ◽  
Vol 207 (1) ◽  
pp. 9-11 ◽  
Author(s):  
Robert S. Fischer

Polarized epithelial cells create tightly packed arrays of microvilli in their apical membrane, but the fate of these microvilli is relatively unknown when epithelial cell polarity is lost during wound healing. In this issue, Klingner et al. (2014. J. Cell Biol. http://dx.doi.org/10.1083/jcb.201402037) show that, when epithelial cells become subconfluent, actomyosin contractions locally within the apical cortex cause their microvilli to become motile over the dorsal/apical surface. Their unexpected observations may have implications for epithelial responses in wound healing and disease.


2013 ◽  
Vol 24 (7) ◽  
pp. 945-963 ◽  
Author(s):  
Wangsun Choi ◽  
Nathan J. Harris ◽  
Kaelyn D. Sumigray ◽  
Mark Peifer

The establishment and maintenance of apical–basal cell polarity is critical for assembling epithelia and maintaining organ architecture. Drosophila embryos provide a superb model. In the current view, apically positioned Bazooka/Par3 is the initial polarity cue as cells form during cellularization. Bazooka then helps to position both adherens junctions and atypical protein kinase C (aPKC). Although a polarized cytoskeleton is critical for Bazooka positioning, proteins mediating this remained unknown. We found that the small GTPase Rap1 and the actin-junctional linker Canoe/afadin are essential for polarity establishment, as both adherens junctions and Bazooka are mispositioned in their absence. Rap1 and Canoe do not simply organize the cytoskeleton, as actin and microtubules become properly polarized in their absence. Canoe can recruit Bazooka when ectopically expressed, but they do not obligatorily colocalize. Rap1 and Canoe play continuing roles in Bazooka localization during gastrulation, but other polarity cues partially restore apical Bazooka in the absence of Rap1 or Canoe. We next tested the current linear model for polarity establishment. Both Bazooka and aPKC regulate Canoe localization despite being “downstream” of Canoe. Further, Rap1, Bazooka, and aPKC, but not Canoe, regulate columnar cell shape. These data reshape our view, suggesting that polarity establishment is regulated by a protein network rather than a linear pathway.


2008 ◽  
Vol 283 (34) ◽  
pp. 23440-23449 ◽  
Author(s):  
Wei Feng ◽  
Hao Wu ◽  
Ling-Nga Chan ◽  
Mingjie Zhang

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Alessia Caramello ◽  
Christophe Galichet ◽  
Karine Rizzoti ◽  
Robin Lovell-Badge

During embryonic development, radial glial cells give rise to neurons, then to astrocytes following the gliogenic switch. Timely regulation of the switch, operated by several transcription factors, is fundamental for allowing coordinated interactions between neurons and glia. We deleted the gene for one such factor, SOX9, early during mouse brain development and observed a significantly compromised dentate gyrus (DG). We dissected the origin of the defect, targeting embryonic Sox9 deletion to either the DG neuronal progenitor domain or the adjacent cortical hem (CH). We identified in the latter previously uncharacterized ALDH1L1+ astrocytic progenitors, which form a fimbrial-specific glial scaffold necessary for neuronal progenitor migration towards the developing DG. Our results highlight an early crucial role of SOX9 for DG development through regulation of astroglial potential acquisition in the CH. Moreover, we illustrate how formation of a local network, amidst astrocytic and neuronal progenitors originating from adjacent domains, underlays brain morphogenesis.


2018 ◽  
pp. 51-71
Author(s):  
Arthur J. Molendijk ◽  
Olaf Tietz ◽  
Benedetto Ruperti ◽  
Ivan A. Paponov ◽  
Klaus Palme

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