The Regenerating Adult Zebrafish Retina Recapitulates Developmental Fate Specification Programs.
The Regenerating Adult Zebrafish Retina Recapitulates Developmental Fate Specification Programs.
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DOI：
10.3389/fcell.2020.617923
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发表时间：
2020
影响因子：
5.5
通讯作者：
Hyde DR
中科院分区：
文献类型：
--
作者：
Lahne M;Brecker M;Jones SE;Hyde DR
成年斑马鱼具有显著的再生神经元的能力。在受损的斑马鱼视网膜中，Müler神经胶质细胞重新编程和分裂，产生神经前体细胞(NC)，增殖和分化为丢失的和不受损伤刺激影响的神经细胞类型，这表明发育规范/分化程序可能在再生过程中重现。实时定量聚合酶链式反应显示，发育能力因子在强光诱导的光感受器损伤后或在遗传杆光感受器细胞消融模型中表达。在光和N-甲基-D-天冬氨酸(NMDA)损伤的成年斑马鱼视网膜中，NPC表达由神经节启动子(Atoh7)、无长突(Ptf1a)、双极(Vsx1)或红锥感光细胞能力因子(Thrb)控制的荧光报告，而不是增殖的Müller胶质细胞。在两种损伤模式中，toh7：GFP首先表达，然后是ptf1a：EGFP，最后是vsx1：gfp，而thrb：番茄在光损伤后与ptf1a：gfp同时在NPC中表达，但在NMDA损伤的视网膜中与vsx1：gfp一起移动。此外，代表神经节和无长突细胞分化的Huc/D在两种损伤范例中均先与atoh7：GFP共定位于神经节细胞层，然后在THEB：番茄外核层表达ZPR-1(红色/绿色锥状光感受器)，模拟发育分化顺序。然而，与光损伤视网膜相比，表达atoh7：GFP的增殖细胞核抗原阳性细胞比例增加，表达thrB：番茄和vsx1：GFP的比例降低，而表达ptf1a：GFP的比例不变。综上所述，在视网膜再生过程中概述了发育细胞规范程序，以适应细胞类型的丢失。
Adult zebrafish possess the remarkable capacity to regenerate neurons. In the damaged zebrafish retina, Müller glia reprogram and divide to produce neuronal progenitor cells (NPCs) that proliferate and differentiate into both lost neuronal cell types and those unaffected by the damage stimulus, which suggests that developmental specification/differentiation programs might be recapitulated during regeneration. Quantitative real-time polymerase chain reaction revealed that developmental competence factors are expressed following photoreceptor damage induced by intense light or in a genetic rod photoreceptor cell ablation model. In both light- and N-Methyl-D-aspartic acid (NMDA)-damaged adult zebrafish retinas, NPCs, but not proliferating Müller glia, expressed fluorescent reporters controlled by promoters of ganglion (atoh7), amacrine (ptf1a), bipolar (vsx1), or red cone photoreceptor cell competence factors (thrb) in a temporal expression sequence. In both damage paradigms, atoh7:GFP was expressed first, followed by ptf1a:EGFP and lastly, vsx1:GFP, whereas thrb:Tomato was observed in NPCs at the same time as ptf1a:GFP following light damage but shifted alongside vsx1:GFP in the NMDA-damaged retina. Moreover, HuC/D, indicative of ganglion and amacrine cell differentiation, colocalized with atoh7:GFP prior to ptf1a:GFP expression in the ganglion cell layer, which was followed by Zpr-1 expression (red/green cone photoreceptors) in thrb:Tomato-positive cells in the outer nuclear layer in both damage paradigms, mimicking the developmental differentiation sequence. However, comparing NMDA- to light-damaged retinas, the fraction of PCNA-positive cells expressing atoh7:GFP increased, that of thrb:Tomato and vsx1:GFP decreased, and that of ptf1a:GFP remained similar. To summarize, developmental cell specification programs were recapitulated during retinal regeneration, which adapted to account for the cell type lost.
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影响因子：
3.6
作者：
Feng L;Xie ZH;Ding Q;Xie X;Libby RT;Gan L
通讯作者：
Gan L
影响因子：
--
作者：
Fossat, Nicolas;Le Greneur, Coralie;Beby, Francis;Vincent, Stephane;Godement, Pierre;Chatelain, Gilles;Lamonerie, Thomas
通讯作者：
Lamonerie, Thomas
影响因子：
5.3
作者：
Bernardos, Rebecca L.;Barthel, Linda K.;Raymond, Pamela A.
通讯作者：
Raymond, Pamela A.
DOI：
10.1111/j.1600-0854.2010.01085.x
发表时间：
2010-09
期刊：
Traffic (Copenhagen, Denmark)
影响因子：
--
作者：
Ile KE;Kassen S;Cao C;Vihtehlic T;Shah SD;Mousley CJ;Alb JG Jr;Huijbregts RP;Stearns GW;Brockerhoff SE;Hyde DR;Bankaitis VA
通讯作者：
Bankaitis VA
影响因子：
5.3
作者：
Baye, Lisa M.;Link, Brian A.
通讯作者：
Link, Brian A.