Borges Augusto, Pinto-Teixeira Filipe, Wibowo Indra, Pogoda Hans-Martin, Hammerschmidt Matthias, Kawakami Koichi, López-Schier Hernán, Miranda-Rodríguez Jerónimo Roberto
Graduate School of Quantitative Biosciences, Ludwig-Maximilians-Universität München, Munich, Germany.
Center for Developmental Biology, Université Toulouse III - Paul Sabatier, Toulouse, France.
MicroPubl Biol. 2024 Sep 23;2024. doi: 10.17912/micropub.biology.001342. eCollection 2024.
Mutations in cause branchio-oto-renal syndrome (BOR) in humans and the equivalent condition in animal models. BOR is characterized by multi-organ malformations. To better understand the role of Eya1 in organogenesis we used the zebrafish posterior lateral-line primordium. This multicellular tissue moves from head-to-tail at a constant velocity via the simultaneous action of two chemokine receptors, Cxcr4b and Ackr3b (formerly cxcr7b). We found that loss of strongly reduces the expression of , disrupting the coherent motion of the primordium and leading to lateral-line truncations. These findings point to abnormal collective cell chemotaxis as the origin of organ dysmorphia in BOR.
基因的突变会导致人类的鳃耳肾综合征（BOR）以及动物模型中的等效病症。BOR的特征是多器官畸形。为了更好地理解Eya1在器官发生中的作用，我们使用了斑马鱼的后侧线原基。这个多细胞组织通过两种趋化因子受体Cxcr4b和Ackr3b（以前称为cxcr7b）的同时作用，以恒定速度从头部向尾部移动。我们发现该基因的缺失会强烈降低某个基因的表达，破坏原基的连贯运动并导致侧线截断。这些发现表明异常的集体细胞趋化作用是BOR中器官畸形的起源。 （注：原文中部分基因名称缺失，以上译文为尽量完整呈现意思所补充，实际翻译时应根据准确的原文基因名称进行翻译）
