Regulation of Gliogenesis by<i>lin-32</i>/Atoh1 in<i>Caenorhabditis elegans</i>

Zhang, Albert; Noma, Kentaro; Yan, Dong

doi:10.1534/g3.120.401547

Cited by 16 publications

(16 citation statements)

References 60 publications

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“…Furthermore, these glial cells are vital for the proper functioning of the neurons that they ensheath, where they can modulate neural activity through secreted molecules at the receptive endings and control neuron receptive ending shape ( Bacaj et al, 2008 ; Shaham, 2010 ; Singhvi et al, 2016 ). In previous studies we show that the fate determination of C. elegans AMsh glial cells utilizes similar mechanisms as those in mammals ( Zhang et al, 2020a ). AMsh glia are born close to the nose of C. elegans , where their processes anchor to the nose region while the cell bodies migrate toward the nerve ring ( Shaham, 2015 ; Heiman and Shaham, 2009 ), and the position of AMsh glia is important for their function ( Zhang et al, 2020b ).…”

Section: Introductionmentioning

confidence: 73%

Robo functions as an attractive cue for glial migration through SYG-1/Neph

Zhang

Yan

2020

eLife

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As one of the most-studied receptors, Robo plays functions in many biological processes, and its functions highly depend on Slit, the ligand of Robo. Here we uncover a Slit-independent role of Robo in glial migration and show that neurons can release an extracellular fragment of Robo upon cleavage to attract glia during migration in Caenorhabditis elegans. Furthermore, we identified the conserved cell adhesion molecule SYG-1/Neph as a receptor for the cleaved extracellular Robo fragment to mediate glial migration and SYG-1/Neph functions through regulation of the WAVE complex. Our studies reveal a previously unknown Slit-independent function and regulatory mechanism of Robo and show that the cleaved extracellular fragment of Robo can function as a ligand for SYG-1/Neph to guide glial migration. As Robo, the cleaved region of Robo, and SYG-1/Neph are all highly conserved across the animal kingdom, our findings may present a conserved Slit-independent Robo mechanism during brain development.

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Section: Introductionmentioning

confidence: 73%

Robo functions as an attractive cue for glial migration through SYG-1/Neph

Zhang

Yan

2020

eLife

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“…Four neurons (AWA, AWB, AWC, AFD) form elaborate ciliated endings that are embedded in the wing-shaped portion of the sheath, while the others (ASE, ADF, ASG, ASH, ASI, ASJ, ASK, ADL) terminate in simple cilia that lie in a central lumenal channel [27,30]. Previous genetic screens have identified mutants that affect amphid sheath specification and cell body positioning [31], that disrupt extension of the amphid sheath glial process [9,22], or that lead to enlarged or supernumerary amphid sheath cells [32,33].…”

Section: Resultsmentioning

confidence: 99%

Loss of the extracellular matrix protein DIG-1 causes glial fragmentation, dendrite breakage, and dendrite extension defects

Chong

Cebul

Mizeracka

et al. 2021

Preprint

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The extracellular matrix (ECM) guides and constrains the shape of the nervous system. In C. elegans, DIG-1 is a giant ECM component that is required for fasciculation of sensory dendrites during development and for maintenance of axon positions throughout life. We identified four novel alleles of dig-1 in three independent screens for mutants affecting disparate aspects of neuronal and glial morphogenesis. First, we find that disruption of DIG-1 causes fragmentation of the amphid sheath glial cell in larvae and young adults. Second, it causes severing of the BAG sensory dendrite from its terminus at the nose tip, apparently due to breakage of the dendrite as animals reach adulthood. Third, it causes embryonic defects in dendrite fasciculation in inner labial (IL2) sensory neurons, as previously reported, as well as rare defects in IL2 dendrite extension that are enhanced by loss of the apical ECM component DYF-7, suggesting that apical and basolateral ECM contribute separately to dendrite extension. Our results highlight novel roles for DIG-1 in maintaining the cellular integrity of neurons and glia, possibly by creating a barrier between structures in the nervous system.

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“…NeuroD1 have been shown to regulate neuron-glia fate determination, where they independently promote a neuronal fate while suppressing a glial fate [27][28][29]. Recent studies in C. elegans show that loss of function of the Neurog1 and NeuroD1 orthologs, ngn-1 and cnd-1 respectively, also result in an increase in the number of AMsh glia, which is consistent with a suppression of glial fate [22]. It was also found that LIN-32, an ortholog of the proneural gene Atoh1, functioned similarly.…”

Section: For Example Several Conserved Proneural Transcription Factomentioning

confidence: 97%

“…This article is protected by copyright. All rights reserved glia in lin-32 loss of function mutants came from cells originally fated to become CEPsh glia, suggesting that this proneural transcription factor may also play a role in glial identity specification [22].…”

Section: Accepted Articlementioning

confidence: 99%

C. elegans as a model to study glial development

Zhang

Yan

2021

The FEBS Journal

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Glia make up roughly half of all cells in the mammalian nervous system and play a major part in nervous system development, function and disease. Although research in the past few decades have shed light on their morphological and functional diversity, there is still much to be known about key aspects of their development such as the generation of glial diversity and the factors governing proper morphogenesis. Glia of the nematode C. elegans possess many developmental and morphological similarities with their vertebrate counterparts and can potentially be used as a model to understand certain aspects of glial biology owing to advantages such as its genetic tractability and fully mapped cell lineage. In this review we summarize recent progress in our understanding of genetic pathways that regulate glial development in C. elegans and discuss how some of these findings may be conserved.

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Regulation of Gliogenesis bylin-32/Atoh1 inCaenorhabditis elegans

Cited by 16 publications

References 60 publications

Robo functions as an attractive cue for glial migration through SYG-1/Neph

Robo functions as an attractive cue for glial migration through SYG-1/Neph

Loss of the extracellular matrix protein DIG-1 causes glial fragmentation, dendrite breakage, and dendrite extension defects

C. elegans as a model to study glial development

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