RT Journal Article
SR Electronic
T1 GJA1 Depletion Causes Ciliary Defects by Affecting Rab11 Trafficking to the Ciliary Base
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 2020.11.13.381764
DO 10.1101/2020.11.13.381764
A1 Dong Gil Jang
A1 Keun Yeong Kwon
A1 Yeong Cheon Kweon
A1 Byung-gyu Kim
A1 Kyungjae Myung
A1 Hyun-Shik Lee
A1 Chan Young Park
A1 Taejoon Kwon
A1 Tae Joo Park
YR 2020
UL http://biorxiv.org/content/early/2020/11/16/2020.11.13.381764.abstract
AB The gap junction complex functions as a transport channel across the membrane. Among gap junction subunits, gap junction protein alpha 1 (GJA1) is the most commonly expressed subunit. However, the roles of GJA1 in the formation and function of cilia remain unknown. Here, we examined GJA1 functions during ciliogenesis in vertebrates. GJA1 was localized to the motile ciliary axonemes or pericentriolar material (PCM) around the primary cilium. GJA1 depletion caused the severe malformation of both primary cilium and motile cilia. Interestingly, GJA1 depletion caused strong delocalization of BBS4 from the PCM and basal body and distinct distribution as cytosolic puncta. Further, CP110 removal from the mother centriole was significantly reduced by GJA1 depletion. Importantly, Rab11, key regulator during ciliogenesis, was immunoprecipitated with GJA1 and GJA1 knockdown caused the mis-localization and mis-accumulation of Rab11. These findings suggest that GJA1 is necessary for proper ciliogenesis by regulating the Rab11 pathway.