SOI1 encodes a novel, conserved protein that promotes TGN-endosomal cycling of Kex2p and other membrane proteins by modulating the function of two TGN localization signals.
SOI1 encodes a novel, conserved protein that promotes TGN-endosomal cycling of Kex2p and other membrane proteins by modulating the function of two TGN localization signals.
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DOI：
10.1083/jcb.139.1.23
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发表时间：
1997-10-06
影响因子：
7.8
通讯作者：
Fuller, RS
中科院分区：
文献类型：
--
作者：
Brickner, JH;Fuller, RS
酵母Kex2蛋白酶定位到TGN需要在其胞质尾部（C-tail）有一个信号（TLS1）。TLS1突变导致Kex2p快速转运到液泡。TLS1中Tyr713Ala突变抑制子的分离先前鉴定了三个SOI基因。SOI1通过孢子缺陷的互补克隆，编码了一种新的亲水性3144 -残基蛋白，在秀丽隐杆线虫、黑腹果蝇和人类中具有同源物。表位标记的Soi1p以洗涤剂不敏感、可沉积的形式存在。SOI1的缺失破坏了野生型Kex2p和含有Ste13p c尾的融合蛋白的TGN定位，并导致羧基肽酶Y的错误分选，加速Vps10p分选受体的空泡降解。SOI1的缺失改善了Tyr713Ala Kex2p在前α-因子加工区中的保留，但与原始SOI1等位基因不同，并没有增加Tyr713Ala Kex2p的半衰期。这些结果表明，Soi1p在TGN和泡前室（PVC）之间的Kex2p和其他蛋白质循环中起两个步骤的作用。这个假设在几个方面得到了证实。Soi1p被证明是TLS1的最佳功能所必需的。SOI1突变对Tyr713Ala突变的抑制是通过激活Kex2p c尾的第二个信号（TLS2）引起的。TLS2延迟了ke2p从TGN的退出，而TLS1对这一步没有影响。我们提出Soi1p通过拮抗TGN保留信号（TLS2）和促进作用于PVC的恢复信号（TLS1）的功能，促进TGN膜蛋白在TGN和PVC之间的循环。
Localization of yeast Kex2 protease to the TGN requires a signal (TLS1) in its cytosolic tail (C-tail). Mutation of TLS1 results in rapid transit of Kex2p to the vacuole. Isolation of suppressors of the Tyr713Ala mutation in TLS1 previously identified three SOI genes. SOI1, cloned by complementation of a sporulation defect, encodes a novel, hydrophilic 3,144-residue protein with homologues in Caenorhabditis elegans, Drosophila melanogaster, and humans. Epitope-tagged Soi1p existed in a detergent-insensitive, sedimentable form. Deletion of SOI1 impaired TGN localization of wild-type Kex2p and a fusion protein containing the C-tail of Ste13p, and also caused missorting of carboxypeptidase Y and accelerated vacuolar degradation of the Vps10p sorting receptor. Deletion of SOI1 improved retention of Tyr713Ala Kex2p in the pro-α-factor processing compartment but, unlike the original soi1 alleles, did not increase the half-life of Tyr713Ala Kex2p. These results suggested that Soi1p functions at two steps in the cycling of Kex2p and other proteins between the TGN and prevacuolar compartment (PVC). This hypothesis was confirmed in several ways. Soi1p was shown to be required for optimal function of TLS1. Suppression of the Tyr713Ala mutation by mutation of SOI1 was shown to be caused by activation of a second signal (TLS2) in the Kex2p C-tail. TLS2 delayed exit of Kex2p from the TGN, whereas TLS1 did not affect this step. We propose that Soi1p promotes cycling of TGN membrane proteins between the TGN and PVC by antagonizing a TGN retention signal (TLS2) and facilitating the function of a retrieval signal (TLS1) that acts at the PVC.
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影响因子：
7.8
作者：
FRANZUSOFF, A;REDDING, K;SCHEKMAN, R
通讯作者：
SCHEKMAN, R
影响因子：
64.5
作者：
JULIUS, D;BRAKE, A;THORNER, J
通讯作者：
THORNER, J
DOI：
10.1083/jcb.119.6.1459
发表时间：
1992-12
期刊：
The Journal of cell biology
影响因子：
--
作者：
Cooper A;Bussey H
通讯作者：
Bussey H
影响因子：
64.5
作者：
MARCUSSON, EG;HORAZDOVSKY, BF;EMR, SD
通讯作者：
EMR, SD
影响因子：
11.4
作者：
CHAPMAN, RE;MUNRO, S
通讯作者：
MUNRO, S