TY - JOUR
T1 - Ypt1/Rab1 regulates Hrr25/CK1δ kinase activity in ER-Golgi traffic and macroautophagy.
AU - Wang, Juan
AU - Davis, Saralin
AU - Menon, Shekar
AU - Zhang, Jinzhong
AU - Ding, Jingzhen
AU - Cervantes, Serena
AU - Miller, Elizabeth
AU - Jiang, Yu
AU - Ferro-Novick, Susan
PY - 2015/7/20
Y1 - 2015/7/20
N2 - ER-derived COPII-coated vesicles are conventionally targeted to the Golgi. However, during cell stress these vesicles also become a membrane source for autophagosomes, distinct organelles that target cellular components for degradation. How the itinerary of COPII vesicles is coordinated on these pathways remains unknown. Phosphorylation of the COPII coat by casein kinase 1 (CK1), Hrr25, contributes to the directional delivery of ER-derived vesicles to the Golgi. CK1 family members are thought to be constitutively active kinases that are regulated through their subcellular localization. Instead, we show here that the Rab GTPase Ypt1/Rab1 binds and activates Hrr25/CK1δ to spatially regulate its kinase activity. Consistent with a role for COPII vesicles and Hrr25 in membrane traffic and autophagosome biogenesis, hrr25 mutants were defective in ER–Golgi traffic and macroautophagy. These studies are likely to serve as a paradigm for how CK1 kinases act in membrane traffic.
AB - ER-derived COPII-coated vesicles are conventionally targeted to the Golgi. However, during cell stress these vesicles also become a membrane source for autophagosomes, distinct organelles that target cellular components for degradation. How the itinerary of COPII vesicles is coordinated on these pathways remains unknown. Phosphorylation of the COPII coat by casein kinase 1 (CK1), Hrr25, contributes to the directional delivery of ER-derived vesicles to the Golgi. CK1 family members are thought to be constitutively active kinases that are regulated through their subcellular localization. Instead, we show here that the Rab GTPase Ypt1/Rab1 binds and activates Hrr25/CK1δ to spatially regulate its kinase activity. Consistent with a role for COPII vesicles and Hrr25 in membrane traffic and autophagosome biogenesis, hrr25 mutants were defective in ER–Golgi traffic and macroautophagy. These studies are likely to serve as a paradigm for how CK1 kinases act in membrane traffic.
UR - http://europepmc.org/abstract/med/26195667
UR - https://www.scopus.com/record/display.uri?eid=2-s2.0-84957649648&origin=inward
U2 - 10.1083/jcb.201408075
DO - 10.1083/jcb.201408075
M3 - Article
C2 - 26195667
SN - 0021-9525
VL - 210
SP - 273
EP - 285
JO - Journal of Cell Biology
JF - Journal of Cell Biology
IS - 2
ER -