Regeneration of myelin sheaths of normal length and thickness in the zebrafish CNS correlates with growth of axons in caliber

Karttunen, Marja J.; Czopka, Tim; Goedhart, Martin; Early, Jason J; Lyons, David A.

doi:10.1371/journal.pone.0178058

Cited by 30 publications

(34 citation statements)

References 98 publications

(110 reference statements)

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“…We used the following existing zebrafish lines and strains: Tg(mbp:nls-EGFP) 48 , Tg(mbp:EGFP-CAAX) ue2Tg 49 , Tg(mbpa:MA-Cerulean) tm101Tg 30 (here referred to as Tg(mbp:memCerulean), Tg(elavl3:HSA.h2b-GCaMP6s) jf5Tg 50 (here referred to as Tg(elavl3:h2b-GCaMP6s), nacre and AB. The following lines were newly generated for this study: Tg(mfap4:memCerulean), Tg(olig1:GCaMP6m), Tg(olig1:KalTA4), Tg(olig1:memEYFP), Tg(olig1:nls-Cerulean), Tg(olig1:nls-mApple), Tg(mbp:KillerRed), Tg(elavl3:synaptophysin-tagRFP).…”

Section: Methods Detailsmentioning

confidence: 99%

Functionally distinct subgroups of oligodendrocyte precursor cells integrate neural activity and execute myelin formation

et al. 2020

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Recent reports have revealed oligodendrocyte precursor cell (OPC) heterogeneity. It remains unclear if such heterogeneity reflects different subtypes of cells with distinct functions, or rather transiently acquired states of cells with the same function. By integrating lineage formation of individual OPC clones, single-cell transcriptomics, calcium imaging and neural activity manipulation, we show that OPCs in the zebrafish spinal cord can be divided into two functionally distinct groups. One subgroup forms elaborate networks of processes and exhibits a high degree of calcium signalling, but infrequently differentiates, despite contact with permissive axons. Instead, these OPCs divide in an activity and calcium dependent manner to produce another subgroup with higher process motility and less calcium signaling, which readily differentiates. Our data show that OPC subgroups are functionally diverse in responding to neurons and reveal that activity regulates proliferation of a subset of OPCs that is distinct from the cells that generate differentiated oligodendrocytes.

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Section: Methods Detailsmentioning

confidence: 99%

Functionally distinct subgroups of oligodendrocyte precursor cells integrate neural activity and execute myelin formation

et al. 2020

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“…For the larvae to be used in experiments, 1-phenyl 2-thiourea (Sigma; P7629) was added to the Petri dish at 1 dpf in order to prevent pigmentation; at 5 dpf, larvae were transferred to 600-ml beakers filled with 300 ml of E3 medium, where they started to be fed with powder food once per day until the end of the experiments. The following fish lines were used: Tg( mpeg1:eGFP ) ( Ellett et al, 2011 ), Tg( mbp:eGFP-CAAX ) ( Almeida et al, 2011 ), Tg( mbp:mcherry-CAAX ) ( Mensch et al, 2015 ), Tg( olig1:nls-mApple ) ( Auer et al, 2018 ), Tg( mbp:nls-eGFP ) ( Karttunen et al, 2017 ), Tg( sox10:mRFP ) ( Kirby et al, 2006 ), Tg( mpeg1:mCherry-F ) ( Nguyen-Chi et al, 2014 ), Tg( NF-κb:eGFP ) ( Ogryzko et al, 2014 ), csf1ra j4e1/j4e1 ; csf1rb re01/re01 ( Oosterhof et al, 2018 ), and myd88 hu3568/hu3568 ( van der Vaart et al, 2013 ).…”

Section: Methodsmentioning

confidence: 99%

Pro-inflammatory activation following demyelination is required for myelin clearance and oligodendrogenesis

Cunha

Cantuti-Castelvetri

et al. 2020

Journal of Experimental Medicine

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Remyelination requires innate immune system function, but how exactly microglia and macrophages clear myelin debris after injury and tailor a specific regenerative response is unclear. Here, we asked whether pro-inflammatory microglial/macrophage activation is required for this process. We established a novel toxin-based spinal cord model of de- and remyelination in zebrafish and showed that pro-inflammatory NF-κB–dependent activation in phagocytes occurs rapidly after myelin injury. We found that the pro-inflammatory response depends on myeloid differentiation primary response 88 (MyD88). MyD88-deficient mice and zebrafish were not only impaired in the degradation of myelin debris, but also in initiating the generation of new oligodendrocytes for myelin repair. We identified reduced generation of TNF-α in lesions of MyD88-deficient animals, a pro-inflammatory molecule that was able to induce the generation of new premyelinating oligodendrocytes. Our study shows that pro-inflammatory phagocytic signaling is required for myelin debris degradation, for inflammation resolution, and for initiating the generation of new oligodendrocytes.

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“…Peter BrophyN/ARabbit Anti-MNF2 (Anti-Nfasc186), 1:1000Dr. Peter BrophyN/AGoat Anti-Mouse AlexaFlour 488, 1:1000ThermofisherCat#A-21141, RRID:AB_2535778Goat Anti-Mouse AlexaFlour 594, 1:1000ThermofisherCat#A-21125, RRID:AB_2535767Goat Anti-Mouse AlexaFlour 647, 1:1000ThermofisherCat#A-21240, RRID:AB_2535809Goat Anti-Mouse FITC, 1:100Southern BiotecCat# 1021-02, RRID:AB_2794237Goat Anti-Rabbit AlexaFlour 488, 1:1000Molecular ProbesCat# A-11008, RRID:AB_143165Donkey Anti-Rabbit AlexaFlour 594, 1:1000Jackson ImmunoResearchCat#111-585-14,RRID:AB_2307325 Experimental Models: Organisms/Strains Zebrafish: Tg(mbp:EGFP-CAAX)(Almeida et al., 2011)ZFIN: ZDB-ALT-120103-2Zebrafish: Tg(mbp:nlsEGFP)(Karttunen et al., 2017)Zebrafish: Tg(NBT:DsRed, Synon. Tg(Xla.Tubb:DsRed), zf148Tg(Peri and Nüsslein-Volhard, 2008)ZDB-ALT-081027-2Tg(cntn1b:mCherry)(Czopka et al., 2013)ZDB-TGCONSTRUCT-140610-5Zebrafish: Tg(sox10:KalTA4)(Almeida and Lyons, 2015)N/ATg(cldnk:Gal4)(Münzel et al., 2012)ZDB-TGCONSTRUCT-120207-1Zebrafish: Tg(UAS:Mem-GFP)(Kwan et al., 2007)N/AZebrafish: caspr sa12772 (Kettleborough et al., 2013)ZDB-ALT-130530-311Zebrafish: n fascb ue56 this paperN/AMouse: Nfasc-/-/Nfasc186(Zonta et al., 2011)N/AMouse: Caspr-/-(Gollan et al., 2003)N/A Oligonucleotides Morpholino: ATG-nfascb,TGACAGGAATCCTCCAACACTTCATGene ToolsN/AMorpholino: Human Beta-Globin, Standard Negative Control,CCTCTTACCTCAGTTACAATTTATAGene Tools...…”

Section: Methodsmentioning

confidence: 99%

Oligodendrocyte Neurofascin Independently Regulates Both Myelin Targeting and Sheath Growth in the CNS

et al. 2019

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SummarySelection of the correct targets for myelination and regulation of myelin sheath growth are essential for central nervous system (CNS) formation and function. Through a genetic screen in zebrafish and complementary analyses in mice, we find that loss of oligodendrocyte Neurofascin leads to mistargeting of myelin to cell bodies, without affecting targeting to axons. In addition, loss of Neurofascin reduces CNS myelination by impairing myelin sheath growth. Time-lapse imaging reveals that the distinct myelinating processes of individual oligodendrocytes can engage in target selection and sheath growth at the same time and that Neurofascin concomitantly regulates targeting and growth. Disruption to Caspr, the neuronal binding partner of oligodendrocyte Neurofascin, also impairs myelin sheath growth, likely reflecting its association in an adhesion complex at the axon-glial interface with Neurofascin. Caspr does not, however, affect myelin targeting, further indicating that Neurofascin independently regulates distinct aspects of CNS myelination by individual oligodendrocytes in vivo.

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Regeneration of myelin sheaths of normal length and thickness in the zebrafish CNS correlates with growth of axons in caliber

Cited by 30 publications

References 98 publications

Functionally distinct subgroups of oligodendrocyte precursor cells integrate neural activity and execute myelin formation

Functionally distinct subgroups of oligodendrocyte precursor cells integrate neural activity and execute myelin formation

Pro-inflammatory activation following demyelination is required for myelin clearance and oligodendrogenesis

Oligodendrocyte Neurofascin Independently Regulates Both Myelin Targeting and Sheath Growth in the CNS

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