Ton Quynh V, Iovine M Kathryn
Department of Biological Sciences, 111 Research Drive, Iacocca B217, Lehigh University, Bethlehem, PA, USA.
Genesis. 2013 Feb;51(2):75-82. doi: 10.1002/dvg.22349. Epub 2012 Oct 16.
Gap junction channels mediate direct cell-cell communication via the exchange of second messengers, ions, and metabolites from one cell to another. Mutations in several human connexin (cx) genes, the subunits of gap junction channels, disturb the development and function of multiple tissues/organs. In particular, appropriate function of Cx43 is required for skeletal development in all vertebrate model organisms. Importantly, it remains largely unclear how disruption of gap junctional intercellular communication causes developmental defects. Two groups have taken distinct approaches toward defining the tangible molecular changes occurring downstream of Cx43-based gap junctional communication. Here, these strategies for determining how Cx43 modulates downstream events relevant to skeletal morphogenesis were reviewed.
间隙连接通道通过第二信使、离子和代谢物在细胞间的交换介导直接的细胞间通讯。几种人类连接蛋白（cx）基因（间隙连接通道的亚基）的突变会干扰多个组织/器官的发育和功能。特别是，在所有脊椎动物模型生物中，骨骼发育都需要Cx43的正常功能。重要的是，间隙连接细胞间通讯的破坏如何导致发育缺陷在很大程度上仍不清楚。两组研究人员采取了不同的方法来确定基于Cx43的间隙连接通讯下游发生的切实分子变化。在此，对这些确定Cx43如何调节与骨骼形态发生相关的下游事件的策略进行了综述。
