Oh Young S, Turner R James
Membrane Biology Section, Gene Therapy and Therapeutics Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, DHHS, Bethesda, Maryland 20892-1190, USA.
Biochemistry. 2005 Sep 6;44(35):11821-8. doi: 10.1021/bi0509494.
Mutations of human presenilin 1 (PS1) have been genetically linked to early-onset familial Alzheimer's disease. PS1 contains 10 hydrophobic regions (HRs) sufficiently long to be alpha-helical membrane spanning segments. Most previous topology studies agree that the N-terminus of PS1 is cytosolic and HRs 1-6 span the membrane but HR 7 does not. However, whether HRs 8 and 9 are membrane spanning segments remains controversial. Here we study the topology and biogenesis of this region of PS1 using a reporter gene fusion approach, where portions of the PS1 sequence containing possible membrane spanning segments were fused up- or downstream of a reporter sequence whose translocation into the endoplasmic reticulum could be monitored via its glycosylation. We provide strong evidence, supported by cysteine accessibility studies in full-length PS1, that HRs 8 and 9 are indeed membrane spanning and that the integration of HR 8 into the membrane is dependent on the presence of HR 9. We also explain how our results reconcile previous apparently divergent conclusions regarding the topology of HRs 8 and 9.
人类早老素1(PS1)的突变在遗传学上与早发性家族性阿尔茨海默病相关。PS1包含10个疏水区域(HRs),其长度足以形成α-螺旋跨膜片段。以往大多数拓扑结构研究一致认为,PS1的N端位于胞质内,HRs 1-6跨膜,但HR 7不跨膜。然而,HRs 8和9是否为跨膜片段仍存在争议。在此,我们使用报告基因融合方法研究PS1该区域的拓扑结构和生物发生,即将包含可能跨膜片段的PS1序列部分融合到报告序列的上游或下游,通过报告序列的糖基化来监测其向内质网的转运。我们提供了有力证据,全长PS1的半胱氨酸可及性研究也支持这一证据,即HRs 8和9确实跨膜,且HR 8整合到膜中依赖于HR 9的存在。我们还解释了我们的结果如何调和先前关于HRs 8和9拓扑结构明显不同的结论。