Zebrafish pax5 regulates development of the utricular macula and vestibular function
Zebrafish pax5 regulates development of the utricular macula and vestibular function
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DOI：
10.1002/dvdy.20961
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发表时间：
2006-11-01
影响因子：
2.5
通讯作者：
Riley, Bruce B.
中科院分区：
文献类型：
--
作者：
Kwak, Su-jin;Vemaraju, Shruti;Riley, Bruce B.
斑马鱼的耳泡最初形成只有两个感觉上皮细胞，椭圆囊和囊状斑，主要介导前庭和听觉功能，分别。在这里，我们测试的作用pax 5，这是优先表达在椭圆囊黄斑。pax 5的吗啉代敲低会破坏前庭功能，但不会破坏听力。听神经节（SAG）的神经元发育正常。椭圆囊毛细胞似乎正常形成，但随后发生细胞凋亡，并从耳泡中挤出。SAG的树突在椭圆囊中持续存在，但在毛细胞丢失后变得紊乱。球囊中的毛细胞正常发育和存活。pax 5的耳部表达需要pax 2a和fgf 3，这两种基因突变会导致前庭缺陷，尽管是通过不同的机制。因此，pax 5与fgf 3和pax 2a一起工作以建立和/或维持椭圆囊黄斑，并且对于前庭功能是必不可少的。
The zebrafish otic vesicle initially forms with only two sensory epithelia, the utricular and saccular maculae, which primarily mediate vestibular and auditory function, respectively. Here, we test the role of pax5, which is preferentially expressed in the utricular macula. Morpholino knockdown of pax5 disrupts vestibular function but not hearing. Neurons of the statoacoustic ganglion (SAG) develop normally. Utricular hair cells appear to form normally but a variable number subsequently undergo apoptosis and are extruded from the otic vesicle. Dendrites of the SAG persist in the utricle but become disorganized after hair cell loss. Hair cells in the saccule develop and survive normally. Otic expression of pax5 requires pax2a and fgf3, mutations in which cause vestibular defects, albeit by distinct mechanisms. Thus, pax5 works in conjunction with fgf3 and pax2a to establish and/or maintain the utricular macula and is essential for vestibular function.