Institute of Integrative Cell Biology and Physiology, University of Muenster, Muenster, Germany.
Dev Dyn. 2022 Nov;251(11):1897-1907. doi: 10.1002/dvdy.522. Epub 2022 Sep 15.
During eye development the lens placode invaginates to form the lens pit. Further bending of lens epithelium and separation from ectoderm leads eventually to a spherical lens vesicle with enclosed extracellular fluid. Changes in epithelial morphology involve the actin cytoskeleton and its regulators. The myosin Myo9b is simultaneously an actin-based motor and Rho GTPase-activating protein that regulates actin cytoskeleton organization. Myo9b-deficient adult mice and embryos were analyzed for eye malformations and alterations in lens development.
Myo9b-deficient mice showed a high incidence of microphthalmia and cataracts with occasional blepharitis. Formation of the lens vesicle during embryonic lens development was disordered in virtually all embryos. Lens placode invagination was less deep and gave rise to a conical structure instead of a spherical pit. At later stages either no lens vesicle was formed or a significantly smaller one that was not enclosed by the optic cup. Expression of the cell fate marker Pax6 was not altered. Staining of adherens junctions and F-actin was most intense at the tip of conical invaginations, suggesting that mechanical forces are not properly coordinated between epithelial cells that form the pit.
Myo9b is a critical regulator of ocular lens vesicle morphogenesis during eye development.
在眼睛发育过程中,晶状体基板内陷形成晶状体窝。进一步弯曲晶状体上皮细胞并与外胚层分离,最终导致具有封闭细胞外液的球形晶状体泡。上皮形态的变化涉及肌动蛋白细胞骨架及其调节剂。肌球蛋白 Myo9b 既是一种基于肌动蛋白的运动蛋白,也是一种 Rho GTP 酶激活蛋白,可调节肌动蛋白细胞骨架的组织。对 Myo9b 缺陷的成年小鼠和胚胎进行了眼部畸形和晶状体发育改变的分析。
Myo9b 缺陷型小鼠表现出高频率的小眼和白内障,偶尔伴有睑炎。在几乎所有胚胎中,胚胎晶状体发育过程中的晶状体泡形成均出现紊乱。晶状体基板内陷较浅,形成圆锥形结构而不是球形窝。在后期,要么没有形成晶状体泡,要么形成的晶状体泡明显较小,且没有被视杯包围。细胞命运标记物 Pax6 的表达没有改变。黏着连接和 F-肌动蛋白的染色在圆锥形内陷的尖端最为强烈,表明形成窝的上皮细胞之间的机械力没有得到适当协调。
Myo9b 是眼睛发育过程中眼部晶状体泡形态发生的关键调节因子。