Department of Biochemistry and Cell Biology, Stony Brook University, Stony Brook, New York, United States of America.
PLoS One. 2013 Oct 4;8(10):e75782. doi: 10.1371/journal.pone.0075782. eCollection 2013.
The Low-density lipoprotein receptor-Related Protein (LRP) family members are essential for diverse processes ranging from the regulation of gastrulation to the modulation of lipid homeostasis. Receptors in this family bind and internalize a diverse array of ligands in the extracellular matrix (ECM). As a consequence, LRPs regulate a wide variety of cellular functions including, but not limited to lipid metabolism, membrane composition, cell motility, and cell signaling. Not surprisingly, mutations in single human LRPs are associated with defects in cholesterol metabolism and development of atherosclerosis, abnormalities in bone density, or aberrant eye vasculature, and may be a contributing factor in development of Alzheimer's disease. Often, members of this diverse family of receptors perform overlapping roles in the same tissues, complicating the analysis of their function through conventional targeted mutagenesis. Here, we describe development of a mouse Mesd (Mesoderm Development) conditional knockout allele, and demonstrate that ubiquitous deletion of Mesd using Cre-recombinase blocks gastrulation, as observed in the traditional knockout and albino-deletion phenotypes. This conditional allele will serve as an excellent tool for future characterization of the cumulative contribution of LRP members in defined tissues.
低密度脂蛋白受体相关蛋白 (LRP) 家族成员对于从胚胎发生调控到脂质稳态调节的多种过程至关重要。该家族中的受体结合并内化细胞外基质 (ECM) 中各种配体。因此,LRPs 调节多种细胞功能,包括但不限于脂质代谢、膜组成、细胞迁移和细胞信号转导。毫不奇怪,单个人类 LRP 的突变与胆固醇代谢缺陷和动脉粥样硬化的发展、骨密度异常或异常的眼部血管有关,并且可能是阿尔茨海默病发展的一个促成因素。通常,这个多样化的受体家族的成员在相同的组织中发挥重叠的作用,这使得通过传统的靶向突变来分析它们的功能变得复杂。在这里,我们描述了一种小鼠 Mesd(中胚层发育)条件性敲除等位基因的开发,并证明了使用 Cre 重组酶对 Mesd 的普遍缺失阻止了原肠胚形成,就像在传统的敲除和白化缺失表型中观察到的那样。这个条件性等位基因将成为未来在特定组织中对 LRP 成员的累积贡献进行特征描述的出色工具。