【摘 要】
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Foxc1a is a member of forkhead transcription factors.It plays essential roles in vertebrate somitogenesis.However,little is known about the molecular mechanisms underlying its regulation.Using TALENs(
【机 构】
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Model Animal Research Center,MOE Key Laboratory of Model Animal for Disease Study,Nanjing University
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Foxc1a is a member of forkhead transcription factors.It plays essential roles in vertebrate somitogenesis.However,little is known about the molecular mechanisms underlying its regulation.Using TALENs(transcription activator-like effector nucleases),we knocked out foxc1a in zebrafish.Compared to wild type embryos,the foxc1a null embryos exhibited deformed somitegenesis,along with abolished expressions of myoD,fgf8 and deltaC and the significantly increased expression of aldh1a2 in the somitic mesoderm.Knocking down aldh1a2 partially rescued the decreased expressions of myoD,fgf8 and deltaC in foxc1a null embryos.Furthermore,knocking down fgf8 reduced expressions of myoD and deltaC whereas inhibiting Notch signaling decreased expressions of fgf8 and myoD in somitic mesoderm.In contrast,neither knocking down fgf8 nor inhibiting Notch signaling affected the expression of aldh1a2 in somitic mesoderm.Taken together,the results reveal that both Fgf and Notch signaling work downstream of RA signaling to mediate the role of Foxc1a in controlling zebrafish somitogenesis.
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