Neural Regeneration Research ›› 2023, Vol. 18 ›› Issue (2): 445-450.doi: 10.4103/1673-5374.346550

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Sox11b regulates the migration and fate determination of Müller glia-derived progenitors during retina regeneration in zebrafish

Kaida Song1, #, Zihao Lin1, #, Lining Cao2, #, Bowen Lu1, Yuxi Chen1, Shuqiang Zhang1, Jianfeng Lu2, *, Hui Xu1, *   

  1. 1Key Lab of Neuroregeneration of Jiangsu and Ministry of Education, Co-innovation Center of Neuroregeneration, NMPA Key Laboratory for Research and Evaluation of Tissue Engineering Technology Products, Nantong University, Nantong, Jiangsu Province, China; 2Shanghai YangZhi Rehabilitation Hospital (Shanghai Sunshine Rehabilitation Center), Frontier Science Center for Stem Cell Research, School of Life Sciences and Technology, Tongji University, Shanghai, China
  • Online:2023-02-15 Published:2022-08-09
  • Contact: Hui Xu, MD, PhD, huixu82@126.com; Jianfeng Lu, PhD, lu.jianfeng@tongji.edu.cn.
  • Supported by:
    This work was supported by the National Key Research and Development Project of China, Nos. 2017YFA0104100 (to JL), 2017YFA0701304 (to HX); and National Natural Science Foundation of China Nos. 81970820 (to HX), 31930068 (to JL).

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Abstract: The transcription factor Sox11 plays important roles in retinal neurogenesis during vertebrate eye development. However, its function in retina regeneration remains elusive. Here we report that Sox11b, a zebrafish Sox11 homolog, regulates the migration and fate determination of Müller glia-derived progenitors (MGPCs) in an adult zebrafish model of mechanical retinal injury. Following a stab injury, the expression of Sox11b was induced in proliferating MGPCs in the retina. Sox11b knockdown did not affect MGPC formation at 4 days post-injury, although the nuclear morphology and subsequent radial migration of MGPCs were altered. At 7 days post-injury, Sox11b knockdown resulted in an increased proportion of MGPCs in the inner retina and a decreased proportion of MGPCs in the outer nuclear layer, compared with controls. Furthermore, Sox11b knockdown led to reduced photoreceptor regeneration, while it increased the numbers of newborn amacrines and retinal ganglion cells. Finally, quantitative polymerase chain reaction analysis revealed that Sox11b regulated the expression of Notch signaling components in the retina, and Notch inhibition partially recapitulated the Sox11b knockdown phenotype, indicating that Notch signaling functions downstream of Sox11b. Our findings imply that Sox11b plays key roles in MGPC migration and fate determination during retina regeneration in zebrafish, which may have critical implications for future explorations of retinal repair in mammals.

Key words: cell migration, fate determination, Müller glia, Müller glia-derived progenitor, Notch signaling, photoreceptor, retina regeneration, Sox11, transcription factor, zebrafish