Abstract：
BACKGROUND: Meis family of transcription factors operates in Pbx-Meis-Hox regulatory network controlling development of various tissues including eye, limbs, heart, hindbrain or craniofacial skeletal elements originating from the neural crest. Although studies in mouse provide abundant information about Meis factors function in embryogenesis, little is known about their role in zebrafish.
RESULTS: We generated zebrafish lines carrying null mutations in meis1a, meis1b, meis2a, and meis2b genes. Only meis1b mutants are lethal at larval stage around 13 dpf whereas the other mutant lines are viable and fertile. We focused on development of neural crest-derived craniofacial structures such as tendons, cranial nerves, cartilage and accompanying muscles. Meis1b mutants displayed morphogenetic abnormalities in the cartilage originating from the first and second pharyngeal arches. Meckel\'s cartilage was shorter and wider with fused anterior symphysis and abnormal chondrocyte organization. This resulted in impaired tendons and muscle fiber connections while tenocyte development was not largely affected.
CONCLUSIONS: Loss-of-function mutation in meis1b affects cartilage morphology in the lower jaw that leads to disrupted organization of muscles and tendons.
RESULTS: We generated zebrafish lines carrying null mutations in meis1a, meis1b, meis2a, and meis2b genes. Only meis1b mutants are lethal at larval stage around 13 dpf whereas the other mutant lines are viable and fertile. We focused on development of neural crest-derived craniofacial structures such as tendons, cranial nerves, cartilage and accompanying muscles. Meis1b mutants displayed morphogenetic abnormalities in the cartilage originating from the first and second pharyngeal arches. Meckel\'s cartilage was shorter and wider with fused anterior symphysis and abnormal chondrocyte organization. This resulted in impaired tendons and muscle fiber connections while tenocyte development was not largely affected.
CONCLUSIONS: Loss-of-function mutation in meis1b affects cartilage morphology in the lower jaw that leads to disrupted organization of muscles and tendons.
摘要：
背景：Meis家族转录因子在Pbx-Meis-Hox调控网络中运作，控制包括眼睛在内的各种组织的发育，四肢,心,源自神经c的后脑或颅面骨骼元素。尽管在小鼠中的研究提供了关于Meis因子在胚胎发生中起作用的丰富信息，人们对它们在斑马鱼中的作用知之甚少。
结果：我们产生了在meis1a中携带无效突变的斑马鱼品系，meis1b,meis2a,和meis2b基因。只有meis1b突变体在13dpf左右的幼虫阶段是致命的，而其他突变品系是可行和可育的。我们专注于神经cast衍生的颅面结构的发展，例如肌腱，颅神经,软骨和伴随的肌肉。Meis1b突变体在源自第一和第二咽弓的软骨中显示出形态发生异常。Meckel的软骨较短，较宽，前联合融合和软骨细胞组织异常。这导致肌腱和肌纤维连接受损，而肌腱细胞的发育并未受到很大影响。
结论：meis1b的功能缺失突变影响下颌软骨形态，导致肌肉和肌腱组织破坏。
结果：我们产生了在meis1a中携带无效突变的斑马鱼品系，meis1b,meis2a,和meis2b基因。只有meis1b突变体在13dpf左右的幼虫阶段是致命的，而其他突变品系是可行和可育的。我们专注于神经cast衍生的颅面结构的发展，例如肌腱，颅神经,软骨和伴随的肌肉。Meis1b突变体在源自第一和第二咽弓的软骨中显示出形态发生异常。Meckel的软骨较短，较宽，前联合融合和软骨细胞组织异常。这导致肌腱和肌纤维连接受损，而肌腱细胞的发育并未受到很大影响。
结论：meis1b的功能缺失突变影响下颌软骨形态，导致肌肉和肌腱组织破坏。
