Cue1p is an activator of Ubc7p E2 activity in vitro and in vivo

被引:50
作者
Bazirgan, Omar A. [1 ]
Hampton, Randolph Y. [1 ]
机构
[1] Univ Calif San Diego, Sect Cell & Dev Biol, Div Biol Sci, La Jolla, CA 92093 USA
关键词
D O I
10.1074/jbc.M801122200
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Ubc7p is a ubiquitin-conjugating enzyme (E2) that functions with endoplasmic reticulum (ER)-resident ubiquitin ligases (E3s) to promote endoplasmic reticulum-associated degradation (ERAD). Ubc7p only functions in ERAD if bound to the ER surface by Cue1p, a membrane-anchored ER protein. The role of Cue1p was thought to involve passive concentration of Ubc7p at the surface of the ER. However, our biochemical studies of Ubc7p suggested that Cue1p may, in addition, stimulate Ubc7p E2 activity. We have tested this idea and found it to be true both in vitro and in vivo. Ubc7p bound to the soluble domain of Cue1p showed strongly enhanced in vitro ubiquitination activity, both in the presence and absence of E3. Cue1p also enhanced Ubc7p function in vivo, and this activation was separable from the established ER-anchoring role of Cue1p. Finally, we tested in vivo activation of Ubc7p by Cue1p in an assay independent of the ER membrane and ERAD. A chimeric E2 linking Ubc7p to the Cdc34p/Ubc3p localization domain complemented the cdc34-2 TS phenotype, and co-expression of the soluble Cue1p domain enhanced complementation by this chimeric Ubc7p E2. These studies reveal a previously unobserved stimulation of Ubc7p E2 activity by Cue1p that is critical for full ERAD and that functions independently of the well known Cue1p anchoring function. Moreover, it suggests a previously unappreciated mode for regulation of E2s by Cue1p-like interacting partners.
引用
收藏
页码:12797 / 12810
页数:14
相关论文
共 57 条
  • [1] Distinct regulation of Ubc13 functions by the two ubiquitin-conjugating enzyme variants Mms2 and Uev1A
    Andersen, PL
    Zhou, HL
    Pastushok, L
    Moraes, T
    McKenna, S
    Ziola, B
    Ellison, MJ
    Dixit, VM
    Xiao, W
    [J]. JOURNAL OF CELL BIOLOGY, 2005, 170 (05) : 745 - 755
  • [2] Hrd1p/Der3p is a membrane-anchored ubiquitin ligase required for ER-associated degradation
    Bays, NW
    Gardner, RG
    Seelig, LP
    Joazeiro, CA
    Hampton, RY
    [J]. NATURE CELL BIOLOGY, 2001, 3 (01) : 24 - 29
  • [3] Determinants of RING-E2 fidelity for Hrd1p, a membrane-anchored ubiquitin ligase
    Bazirgan, Omar A.
    Garza, Renee M.
    Hampton, Randolph Y.
    [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 2006, 281 (51) : 38989 - 39001
  • [4] Role of Cue1p in ubiquitination and degradation at the ER surface
    Biederer, T
    Volkwein, C
    Sommer, T
    [J]. SCIENCE, 1997, 278 (5344) : 1806 - 1809
  • [5] Distinct ubiquitin-ligase complexes define convergent pathways for the degradation of ER proteins
    Carvalho, Pedro
    Goder, Veit
    Rapoport, Tom A.
    [J]. CELL, 2006, 126 (02) : 361 - 373
  • [6] A MULTIUBIQUITIN CHAIN IS CONFINED TO SPECIFIC LYSINE IN A TARGETED SHORT-LIVED PROTEIN
    CHAU, V
    TOBIAS, JW
    BACHMAIR, A
    MARRIOTT, D
    ECKER, DJ
    GONDA, DK
    VARSHAVSKY, A
    [J]. SCIENCE, 1989, 243 (4898) : 1576 - 1583
  • [7] The activity of a human endoplasmic reticulum-associated degradation E3, gp78, requires its Cue domain,, RING finger, and an E2-binding site
    Chen, B
    Mariano, J
    Tsai, YC
    Chan, AH
    Cohen, M
    Weissman, AM
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2006, 103 (02) : 341 - 346
  • [8] Measuring protein degradation with green fluorescent protein
    Cronin, SR
    Hampton, RY
    [J]. GREEN FLUORESCENT PROTEIN, 1999, 302 : 58 - 73
  • [9] Regulation of HMG-CoA reductase degradation requires the P-type ATPase Cod1p/Spf1p
    Cronin, SR
    Khoury, A
    Ferry, DK
    Hampton, RY
    [J]. JOURNAL OF CELL BIOLOGY, 2000, 148 (05) : 915 - 924
  • [10] A luminal surveillance complex that selects misfolded glycoproteins for ER-associated degradation
    Denic, Vladimir
    Quan, Erin M.
    Weissman, Jonathan S.
    [J]. CELL, 2006, 126 (02) : 349 - 359