在胚胎早期發育的過程中，典型Wnt與Nodal訊息傳遞路徑，是調控前-後及背-腹側體軸形成的主要因子之一。而本系的林鼎晏老師，在過去的研究中發現一個，在細胞中會影響典型Wnt或Nodal訊息傳遞路徑新基因，mcrs1。因此本研究將進一步探討mcrs1對於胚胎體軸形成的影響。本研究發現，mcrs1過度表現或突變後，在胚胎發育的過程中會出現體軸的缺陷。並且報導基因分析的結果顯示，mcrs1可能參與典型Wnt訊息傳遞路徑，並具有抑制典型Wnt訊息傳遞路徑活性的能力。在胚胎發育的過程中，典型Wnt訊息會抑制前側與背側的形成，因此透過全胚胎原位雜交，進一步的探討mcrs1過度表現或突變後，對於背側、前側和典型Wnt訊息目標基因表現區域的影響。結果顯示mcrs1突變後，背側基因foxa3與前腦基因otx2的表現區域減少，而典型Wnt訊息目標基因sp5l的表現區域則是擴大，此結果與報導基因分析是一致的，但在mcrs1過度表現後，sp5l表現區域出現未能解釋的顯著擴大。最後藉由β-catenin免疫螢光染色，探討mcrs1過度表現後對於β-catenin表達和核易位的影響。結果顯示胚胎細胞中mcrs1的過度表現，會導致β-catenin表現的下降。本研究結果顯示，mcrs1會抑制典型Wnt訊息傳遞路徑的活性，並影響前-後與背-腹側體軸的形成。

Canonical Wnt signaling and Nodal signaling pathways are currently considered as the two main factors that control the anterior-posterior and dorsal-ventral body axes formation during zebrafish early embryonic development. According to the previous studies, Lin's lab had found a new gene, mcrs1, which may have the potential role to participate in canonical Wnt and Nodal signaling pathways signaling regulation. Therefore, in this study, we would investigate the role of mcrs1 on body axes formation during early embryonic development. In the present study, we found that axis defects in embryos after mcrs1 gain- or loss-of-function. Besides, we utilized reporter assay to clarify whether mcrs1 is involved in which signaling pathways. The result suggested that mcrs1 may be involved in the canonical Wnt signaling pathway. The reporter assay showed that the activity of canonical Wnt signaling was decreased or increased after mcrs1 gain or loss of function, respectively. The canonical Wnt signaling pathway would inhibit the formation of the anterior and dorsal. Hence, we further determined the gene expression pattern of dorsal, anterior, and Wnt target genes after mcrs1 gain- or loss-of-function. The dorsal midline gene foxa3 and Wnt target genes sp5l was decreased and increased after mcrs1 loss of function, respectively. And the forebrain gene otx2 significantly decreased after mcrs1 loss of function. It was consistent with the result of the reporter assay. However, we also found that sp5l aberrant increased after mcrs1 gain of function. Finally, we utilized immunocytochemistry to investigate the β-catenin expression and nuclear translocation after gain-of mcrs1 function. Our results had shown an overall decreased expression of β-catenin after mcrs1 gain-of-function. Collectively, these findings indicate that mcrs1 is critical for the canonical Wnt signaling pathway and axes formation.

吳沛萱，探討微小球蛋白（MSP58）在轉化生長因子（TGF-β）訊息傳遞中所扮演的角色，國立成功大學生物科技與產業科學系碩士論文，2019。
馬郁翔，探討微小球蛋白（MSP58）與Inversin蛋白之間交互作用，國立成功大學生物科技與產業科學系碩士論文，2018。
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