Gilbert A, Jadot M, Leontieva E, Wattiaux-De Coninck S, Wattiaux R
Laboratoire de Chimie Physiologique, Facultés Universitaires Notre-Dame de la Paix, Belgium.
Exp Cell Res. 1998 Jul 10;242(1):144-52. doi: 10.1006/excr.1998.4101.
We have studied the localization of mutant cystic fibrosis transmembrane regulator delta F508CFTR in pancreatic adenocarcinoma cells (CFPAC), which naturally express the mutant protein. Our goal was to investigate whether delta F508CFTR is strictly retained in the endoplasmic reticulum (ER) or alternatively whether it can be transported beyond the ER and reach the endoplasmic reticulum-Golgi intermediate compartment (ERGIC). This compartment, defined by the presence of the 53-kDa protein ERGIC-53, was identified by subcellular fractionation and by immunofluorescence. Part of the delta F508CFTR population and ERGIC-53 showed similar distributions in membrane fractions analyzed on Nycodenz density gradients. Both proteins were present in density fractions distinct from the ones containing the ER marker proteins calnexin and Sec61. Immunofluorescence microscopy of CFPAC cells revealed some colocalization of delta F508CFTR with ERGIC-53. Following incubation of CFPAC cells at 15 degrees C, a condition known to block ER to Golgi transport, both ERGIC-53 and delta F508CFTR subcellular localizations were altered. By contrast, this temperature shift had no effect on the localization of the ER marker Sec61. Our observations indicate that the abnormal protein delta F508CFTR can leak out of the ER and reach the ERGIC. These results support the idea that this intermediate compartment plays a role in the trafficking events leading to retention and finally degradation of the misfolded delta F508CFTR protein.
我们研究了突变型囊性纤维化跨膜调节因子ΔF508CFTR在胰腺腺癌细胞(CFPAC)中的定位,该细胞天然表达这种突变蛋白。我们的目标是研究ΔF508CFTR是否严格保留在内质网(ER)中,或者它是否可以转运到内质网以外并到达内质网-高尔基体中间腔室(ERGIC)。通过亚细胞分级分离和免疫荧光鉴定了这个由53-kDa蛋白ERGIC-53的存在所定义的腔室。在Nycodenz密度梯度上分析的膜组分中,部分ΔF508CFTR群体和ERGIC-53显示出相似的分布。这两种蛋白质都存在于与含有内质网标记蛋白钙连接蛋白和Sec61的密度组分不同的密度组分中。CFPAC细胞的免疫荧光显微镜检查显示ΔF508CFTR与ERGIC-53有一些共定位。在15℃下孵育CFPAC细胞后,已知这种条件会阻断内质网到高尔基体的转运,ERGIC-53和ΔF508CFTR的亚细胞定位都发生了改变。相比之下,这种温度变化对内质网标记物Sec61的定位没有影响。我们的观察结果表明,异常蛋白ΔF508CFTR可以从内质网中泄漏出来并到达ERGIC。这些结果支持了这样一种观点,即这个中间腔室在导致错误折叠的ΔF508CFTR蛋白滞留并最终降解的运输事件中起作用。