Vertebrate Neurogenesis: Cell Polarity

Zolessi, Flavio R.

doi:10.1002/9780470015902.a0000826.pub2

Cited by 4 publications

(4 citation statements)

References 71 publications

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“…Increasing evidence shows that astrocytes act as the most versatile cell type in various CNS functions such as CNS homeostasis, synaptogenesis, synaptic transmission modulation, and neurovascular signaling (Nedergaard et al, 2003 ; Haydon and Carmignoto, 2006 ; Barres, 2008 ; Wang and Bordey, 2008 ; Zolessi, 2009 ; Kimelberg, 2010 ). Among them, the homeostatic support function was the earliest role assigned to astrocytes.…”

Section: Discussionmentioning

confidence: 99%

Genetic Deletion of TREK-1 or TWIK-1/TREK-1 Potassium Channels does not Alter the Basic Electrophysiological Properties of Mature Hippocampal Astrocytes In Situ

Kiyoshi

Wang

et al. 2016

Front. Cell. Neurosci.

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We have recently shown that a linear current-to-voltage (I-V) relationship of membrane conductance (passive conductance) reflects the intrinsic property of K+ channels in mature astrocytes. While passive conductance is known to underpin a highly negative and stable membrane potential (VM) essential for the basic homeostatic function of astrocytes, a complete repertoire of the involved K+ channels remains elusive. TREK-1 two-pore domain K+ channel (K2P) is highly expressed in astrocytes, and covalent association of TREK-1 with TWIK-1, another highly expressed astrocytic K2P, has been reported as a mechanism underlying the trafficking of heterodimer TWIK-1/TREK-1 channel to the membrane and contributing to astrocyte passive conductance. To decipher the individual contribution of TREK-1 and address whether the appearance of passive conductance is conditional to the co-expression of TWIK-1/TREK-1 in astrocytes, TREK-1 single and TWIK-1/TREK-1 double gene knockout mice were used in the present study. The relative quantity of mRNA encoding other astrocyte K+ channels, such as Kir4.1, Kir5.1, and TREK-2, was not altered in these gene knockout mice. Whole-cell recording from hippocampal astrocytes in situ revealed no detectable changes in astrocyte passive conductance, VM, or membrane input resistance (Rin) in either kind of gene knockout mouse. Additionally, TREK-1 proteins were mainly located in the intracellular compartments of the hippocampus. Altogether, genetic deletion of TREK-1 alone or together with TWIK-1 produced no obvious alteration in the basic electrophysiological properties of hippocampal astrocytes. Thus, future research focusing on other K+ channels may shed light on this long-standing and important question in astrocyte physiology.

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Section: Discussionmentioning

confidence: 99%

Genetic Deletion of TREK-1 or TWIK-1/TREK-1 Potassium Channels does not Alter the Basic Electrophysiological Properties of Mature Hippocampal Astrocytes In Situ

Kiyoshi

Wang

et al. 2016

Front. Cell. Neurosci.

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“…Neuronal patterning is the process by which cells in the developing nervous system differentiate into distinct identities and is heavily controlled by several extracellular factors and signaling gradients across the center axis of the nervous system (dorso-ventral, antero-posterior, left-right). Thus, cell polarity is essential for proper asymmetric divisions, leading to neurogenesis, neuronal positioning, and cellular differentiation [ 93 , 94 ]. Many of the driving pathways of neurogenesis, such as Notch, Hh, and Wnt, have been directly connected to primary cilia [ 89 , 95 , 96 , 97 , 98 , 99 ].…”

Section: Cilia-mediated and Calcium-dependent Biological Processesmentioning

confidence: 99%

Primary Cilia and Calcium Signaling Interactions

Saternos

Ley

AbouAlaiwi

2020

IJMS

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The calcium ion (Ca2+) is a diverse secondary messenger with a near-ubiquitous role in a vast array of cellular processes. Cilia are present on nearly every cell type in either a motile or non-motile form; motile cilia generate fluid flow needed for a variety of biological processes, such as left–right body patterning during development, while non-motile cilia serve as the signaling powerhouses of the cell, with vital singling receptors localized to their ciliary membranes. Much of the research currently available on Ca2+-dependent cellular actions and primary cilia are tissue-specific processes. However, basic stimuli-sensing pathways, such as mechanosensation, chemosensation, and electrical sensation (electrosensation), are complex processes entangled in many intersecting pathways; an overview of proposed functions involving cilia and Ca2+ interplay will be briefly summarized here. Next, we will focus on summarizing the evidence for their interactions in basic cellular activities, including the cell cycle, cell polarity and migration, neuronal pattering, glucose-mediated insulin secretion, biliary regulation, and bone formation. Literature investigating the role of cilia and Ca2+-dependent processes at a single-cellular level appears to be scarce, though overlapping signaling pathways imply that cilia and Ca2+ interact with each other on this level in widespread and varied ways on a perpetual basis. Vastly different cellular functions across many different cell types depend on context-specific Ca2+ and cilia interactions to trigger the correct physiological responses, and abnormalities in these interactions, whether at the tissue or the single-cell level, can result in diseases known as ciliopathies; due to their clinical relevance, pathological alterations of cilia function and Ca2+ signaling will also be briefly touched upon throughout this review.

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“…The central nervous system of vertebrates is originated from a polarized, pseudostratified epithelium, which among other features presents a Laminin1-enriched basal lamina, a subapical N-cadherin-based adherens junctions and apical primary cilia (Zolessi, 2016). These neuroepithelial cells are the progenitors for both glial cells and neurons.…”

Section: Introductionmentioning

confidence: 99%

Photoreceptor progenitor dynamics in the zebrafish embryo retina and its modulation by primary cilia and N-cadherin

Aparicio¹,

Rodao²,

Badano³

et al. 2021

Int. J. Dev. Biol.

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Photoreceptors of the vertebrate neural retina are originated from the neuroepithelium, and like other neurons, must undergo cell body translocation and polarity transitions to acquire their final functional morphology, which includes features of neuronal and epithelial cells. We analyzed this process in detail on zebrafish embryos using in vivo confocal microscopy and electron microscopy. Photoreceptor progenitors were labeled by the transgenic expression of EGFP under the regulation of the photoreceptor-specific promoter crx, and structures of interest were disrupted using morpholino oligomers to knock-down specific genes. Photoreceptor progenitors detached from the basal retina at pre-mitotic stages, rapidly retracting a short basal process as the cell body translocated apically. They remained at an apical position indefinitely to form the outer nuclear layer (ONL), initially extending and retracting highly dynamic neurite-like processes, tangential to the apical surface. Many photoreceptor progenitors presented a short apical primary cilium. The number and length of these cilia was gradually reduced until nearly disappearing around 60 hpf. Their disruption by knocking-down ift88 and elipsa caused a notorious defect on basal process retraction. To assess the role of cell adhesion in the organization of photoreceptor progenitors, we knocked-down cdh2/N-cadherin and observed the cell behavior by time-lapse microscopy. The ectopic photoreceptor progenitors initially migrated in an apparent random manner, profusely extending cell processes, until they encountered other cells to establish cell rosettes in which they stayed acquiring the photoreceptor-like polarity. Altogether, our observations indicate a complex regulation of photoreceptor progenitor dynamics to form the retinal ONL, previous to the post-mitotic maturation stages.

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Vertebrate Neurogenesis: Cell Polarity

Cited by 4 publications

References 71 publications

Genetic Deletion of TREK-1 or TWIK-1/TREK-1 Potassium Channels does not Alter the Basic Electrophysiological Properties of Mature Hippocampal Astrocytes In Situ

Genetic Deletion of TREK-1 or TWIK-1/TREK-1 Potassium Channels does not Alter the Basic Electrophysiological Properties of Mature Hippocampal Astrocytes In Situ

Primary Cilia and Calcium Signaling Interactions

Photoreceptor progenitor dynamics in the zebrafish embryo retina and its modulation by primary cilia and N-cadherin

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