Lee Ann-Hwee, Chu Gerald C, Iwakoshi Neal N, Glimcher Laurie H
Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, MA 02115, USA.
EMBO J. 2005 Dec 21;24(24):4368-80. doi: 10.1038/sj.emboj.7600903. Epub 2005 Dec 15.
The secretory function of cells relies on the capacity of the endoplasmic reticulum (ER) to fold and modify nascent polypeptides and to synthesize phospholipids for the subsequent trafficking of secretory proteins through the ER-Golgi network. We have previously demonstrated that the transcription factor XBP-1 activates the expression of certain ER chaperone genes and initiates ER biogenesis. Here, we have rescued the embryonic lethality of XBP-1 deficient fetuses by targeting an XBP-1 transgene selectively to hepatocytes (XBP-1-/-;LivXBP1). XBP-1-/-;LivXBP1 mice displayed abnormalities exclusively in secretory organs such as exocrine pancreas and salivary gland that led to early postnatal lethality from impaired production of pancreatic digestive enzymes. The ER was poorly developed in pancreatic and salivary gland acinar cells, accompanied by decreased expression of ER chaperone genes. Marked apoptosis of pancreatic acinar cells was observed during embryogenesis. Thus, the absence of XBP-1 results in an imbalance between the cargo load on the ER and its capacity to handle it, leading to the activation of ER stress-mediated proapoptotic pathways. These data lead us to propose that XBP-1 is both necessary and sufficient for the full biogenesis of the secretory machinery in exocrine cells.
细胞的分泌功能依赖于内质网(ER)折叠和修饰新生多肽以及合成磷脂的能力,以便随后通过内质网-高尔基体网络运输分泌蛋白。我们之前已经证明,转录因子XBP-1可激活某些内质网伴侣基因的表达并启动内质网的生物发生。在此,我们通过将XBP-1转基因选择性地靶向肝细胞(XBP-1-/-;LivXBP1),挽救了XBP-1缺陷胎儿的胚胎致死性。XBP-1-/-;LivXBP1小鼠仅在分泌器官如外分泌胰腺和唾液腺中表现出异常,这导致出生后早期因胰腺消化酶产生受损而死亡。胰腺和唾液腺腺泡细胞中的内质网发育不良,同时内质网伴侣基因的表达降低。在胚胎发生过程中观察到胰腺腺泡细胞明显凋亡。因此,XBP-1的缺失导致内质网上的货物负载与其处理能力之间的失衡,从而导致内质网应激介导的促凋亡途径的激活。这些数据使我们提出,XBP-1对于外分泌细胞中分泌机制的完全生物发生既是必要的也是充分的。