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<p>The carboxy-terminal postsynaptic density protein 95/discs large protein/zonula occludens 1 (PDZ) ligand of neuronal nitric oxide synthase (nNOS), known as CAPON, can interact with nNOS to influence neuropathological processes. However, the precise mechanism by which CAPON regulates neuronal regeneration remains poorly understood. In this study, we utilized the planarian <i>Dugesia japonica</i>, a model organism renowned for its remarkable regenerative abilities, to investigate this mechanism. First, we cloned the <i>DjCapon</i> gene and performed RNA interference (RNAi) to knock down <i>DjCapon</i> expression in planarians. Our results revealed that <i>DjCapon</i> knockdown impaired neural regeneration, particularly affecting the regeneration of GABAergic neurons. This impairment led to a reduced sensitivity to light in planarians. Furthermore, <i>DjCapon</i> knockdown decreased the activity of nitric oxide synthase (NOS) and reduced the levels of nitric oxide (NO) in planarians. During neural regeneration, the expression of genes associated with the Wnt/Ca<sup>2</sup>⁺ signaling pathway, including <i>DjWnt5a</i>, calcineurin (<i>DjCaln</i>), and calcium/calmodulin-dependent protein kinase II (<i>DjCamKII</i>), was upregulated following <i>DjCapon</i> knockdown. In summary, our findings demonstrate that <i>DjCapon</i> plays a critical role in regulating neural regeneration. <i>DjCapon</i> may modulate the Wnt/Ca<sup>2</sup>⁺ signaling pathway by influencing NOS activity and NO levels. Additionally, the Wnt/Ca<sup>2</sup>⁺ pathway appears to regulate the regeneration of GABAergic neurons and light sensitivity in planarians. These results provide new insights into the mechanism by which CAPON influences neural regeneration and its potential implications for related diseases.</p>

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DjCapon Affects the Neural Regeneration and Light Sensitivity via NO and Wnt5a Signaling in Planarian Dugesia japonica

  • 期刊论文

  • 发表日期：

    2025年4月12日

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  • Wenshuo Xie,
  • Jicheng Qu,
  • Nianhong Xing,
  • Lili Gao,
  • Hongkuan Deng,
  • Dongwu Liu,
  • Qiuxiang Pang

摘要

The carboxy-terminal postsynaptic density protein 95/discs large protein/zonula occludens 1 (PDZ) ligand of neuronal nitric oxide synthase (nNOS), known as CAPON, can interact with nNOS to influence neuropathological processes. However, the precise mechanism by which CAPON regulates neuronal regeneration remains poorly understood. In this study, we utilized the planarian Dugesia japonica, a model organism renowned for its remarkable regenerative abilities, to investigate this mechanism. First, we cloned the DjCapon gene and performed RNA interference (RNAi) to knock down DjCapon expression in planarians. Our results revealed that DjCapon knockdown impaired neural regeneration, particularly affecting the regeneration of GABAergic neurons. This impairment led to a reduced sensitivity to light in planarians. Furthermore, DjCapon knockdown decreased the activity of nitric oxide synthase (NOS) and reduced the levels of nitric oxide (NO) in planarians. During neural regeneration, the expression of genes associated with the Wnt/Ca2⁺ signaling pathway, including DjWnt5a, calcineurin (DjCaln), and calcium/calmodulin-dependent protein kinase II (DjCamKII), was upregulated following DjCapon knockdown. In summary, our findings demonstrate that DjCapon plays a critical role in regulating neural regeneration. DjCapon may modulate the Wnt/Ca2⁺ signaling pathway by influencing NOS activity and NO levels. Additionally, the Wnt/Ca2⁺ pathway appears to regulate the regeneration of GABAergic neurons and light sensitivity in planarians. These results provide new insights into the mechanism by which CAPON influences neural regeneration and its potential implications for related diseases.