Pard3 regulates contact between neural crest cells and the timing of Schwann cell differentiation but is not essential for neural crest migration or myelination

Blasky, Alex J.; Pan, Lingai; Moens, Cecilia B.; Appel, Bruce

doi:10.1002/dvdy.24172

Cited by 32 publications

(29 citation statements)

References 62 publications

(88 reference statements)

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“…To determine if Sox10:zFucci is neural crest‐specific while NCCs are delaminating and migrating, we crossed the Sox10:zFucci line with the Sox10:mRFP line, which is commonly used to label NCCs (Blasky, Pan, Moens, & Appel, ; Leigh et al, ). We performed time‐lapse confocal microscopy of Sox10:zFucci; Sox10:mRFP‐dual positive embryos from 14 to 23 hours post‐fertilization (hpf) or 13 to 28 hpf (Figure b–e; Supporting Information Movies S1 and S2).…”

Section: Resultsmentioning

confidence: 99%

Tracking neural crest cell cycle progression in vivo

Rajan

Gallik

Monaghan

et al. 2018

Genesis

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Analysis of cell cycle entry/exit and progression can provide fundamental insights into stem cell propagation, maintenance, and differentiation. The neural crest is a unique stem cell population in vertebrate embryos that undergoes long-distance collective migration and differentiation into a wide variety of derivatives. Using traditional techniques such as immunohistochemistry to track cell cycle changes in such a dynamic population is challenging, as static time points provide an incomplete spatiotemporal picture. In contrast, the fluorescent, ubiquitination-based cell cycle indicator (Fucci) system provides in vivo readouts of cell cycle progression and has been previously adapted for use in zebrafish. The most commonly used Fucci systems are ubiquitously expressed, making tracking of a specific cell population challenging. Therefore, we generated a transgenic zebrafish line, Tg(-4.9sox10:mAG-gmnn(1/100)-2A-mCherry-cdt1(1/190)), in which the Fucci system is specifically expressed in delaminating and migrating neural crest cells. Here, we demonstrate validation of this new tool and its use in live high-resolution tracking of cell cycle progression in the neural crest and derivative populations.

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Section: Resultsmentioning

confidence: 99%

Tracking neural crest cell cycle progression in vivo

Rajan

Gallik

Monaghan

et al. 2018

Genesis

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“…Wildtype (WT) strains include AB, TAB, and EKK lines (ZIRC) and transgenic lines include sox10: eGFP (Dutton et al, 2008), tg(sox10: memRFP ) vu234 (Blasky et al, 2014) and tg(hsp70l:shha-eGFP) (Shen, et al 2013). Developmental staging followed previously published standards (Kimmel et al, 1995).…”

Section: Methodsmentioning

confidence: 99%

Cdon promotes neural crest migration by regulating N-cadherin localization

Powell

Williams

Hernandez-Lagunas

et al. 2015

Developmental Biology

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Neural crest cells (NCCs) are essential embryonic progenitor cells that are unique to vertebrates and form a remarkably complex and coordinated system of highly motile cells. Migration of NCCs occurs along specific pathways within the embryo in response to both environmental cues and cell-cell interactions within the neural crest population. Here, we demonstrate a novel role for the putative Sonic hedgehog (Shh) receptor and cell adhesion regulator, cdon, in zebrafish neural crest migration. cdon is expressed in developing premigratory NCCs but is downregulated once the cells become migratory. Knockdown of cdon results in aberrant migration of trunk NCCs: crestin positive cells can emigrate out of the neural tube but stall shortly after the initiation of migration. Live cell imaging analysis demonstrates reduced directedness of migration, increased velocity and mispositioned cell protrusions. In addition, transplantation analysis suggests that cdon is required cell-autonomously for directed NCC migration in the trunk. Interestingly, N-cadherin is mislocalized following cdon knockdown suggesting that the role of cdon in NCCs is to regulate N-cadherin localization. Our results reveal a novel role for cdon in zebrafish neural crest migration, and suggest a mechanism by which Cdon is required to localize N-cadherin to the cell membrane in migratory NCCs for directed migration.

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“…We used several wellcharacterized transgenic lines including Tg(olig2:EGFP) and Tg(sox10:T-RFP) (Blasky, Pan, Moens, & Appel, 2014;H. Importantly, we found that the change in mEGFP accumulation in response to bath application of drugs is FIGURE 7 Electron micrograph analysis of myelinated axons following drug treatment.…”

Section: Resultsmentioning

confidence: 99%

“…Thus, it is a useful proxy for altered myelination in vivo in general. We used several wellcharacterized transgenic lines including Tg(olig2:EGFP) and Tg(sox10:T-RFP) (Blasky, Pan, Moens, & Appel, 2014;H. C. Park, Shin, Roberts, & Appel, 2007;Takada et al, 2010); as well as, several reporter lines made with a previously isolated regulatory sequence for mbp1a (Almeida et al, 2011;Jung et al, 2010;, to more closely assess the responses of oligodendrocyte lineage cells to GC1 and rapamycin to better understand the specific impact of each drug on myelination.…”

Section: Figurementioning

confidence: 99%

A novel myelin protein zero transgenic zebrafish designed for rapid readout of in vivo myelination

Preston

Finseth

Bourne

et al. 2019

Glia

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Demyelination occurs following many neurological insults, most notably in multiple sclerosis (MS). Therapeutics that promote remyelination could slow the neurological decline associated with chronic demyelination; however, in vivo testing of candidate small molecule drugs and signaling cascades known to impact myelination is expensive and labor intensive. Here, we describe the development of a novel zebrafish line which uses the putative promoter of Myelin Protein Zero (mpz), a major structural protein in myelin, to drive expression of Enhanced Green Fluorescent Protein (mEGFP) specifically in the processes and nascent internodes of myelinating glia. We observe that changes in fluorescence intensity in Tg(mpz:mEGFP) larvae are a reliable surrogate for changes in myelin membrane production per se in live larvae following bath application of drugs. These changes in fluorescence are strongly predictive of changes in myelin‐specific mRNAs [mpz, 36K and myelin basic protein (mbp)] and protein production (Mbp). Finally, we observe that certain drugs alter nascent internode number and length, impacting the overall amount of myelin membrane synthesized and a number of axons myelinated without significantly changing the number of myelinating oligodendrocytes. These studies demonstrate that the Tg(mpz:mEGFP) reporter line responds effectively to positive and negative small molecule regulators of myelination, and could be useful for identifying candidate drugs that specifically target myelin membrane production in vivo. Combined with high throughput cell‐based screening of large chemical libraries and automated imaging systems, this transgenic line is useful for rapid large scale whole animal screening to identify novel myelinating small molecule compounds in vivo.

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Pard3 regulates contact between neural crest cells and the timing of Schwann cell differentiation but is not essential for neural crest migration or myelination

Cited by 32 publications

References 62 publications

Tracking neural crest cell cycle progression in vivo

Tracking neural crest cell cycle progression in vivo

Cdon promotes neural crest migration by regulating N-cadherin localization

A novel myelin protein zero transgenic zebrafish designed for rapid readout of in vivo myelination

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