TY - JOUR
T1 - Silencing of TBC1D15 promotes RhoA activation and membrane blebbing
AU - Takahara, Yuko
AU - Maeda, Masao
AU - Hasegawa, Hitoki
AU - Ito, Satoko
AU - Hyodo, Toshinori
AU - Asano, Eri
AU - Takahashi, Masahide
AU - Hamaguchi, Michinari
AU - Senga, Takeshi
N1 - Funding Information:
Acknowledgments We would like to thank the members of the Division of Cancer Biology for helpful discussions and technical assistances. This research was partially funded by a grant from the Ministry of Education, Culture, Sports, Science, and Technology of Japan.
PY - 2014/4
Y1 - 2014/4
N2 - Membrane blebs are round-shaped dynamic membrane protrusions that occur under many physiological conditions. Membrane bleb production is primarily controlled by actin cytoskeletal rearrangements mediated by RhoA. Tre2-Bub2-Cdc16 (TBC) domain-containing proteins are negative regulators of the Rab family of small GTPases and contain a highly conserved TBC domain. In this report, we show that the expression of TBC1D15 is associated with the activity of RhoA and the production of membrane blebs. Depletion of TBC1D15 induced activation of RhoA and membrane blebbing, which was abolished by the addition of an inhibitor for RhoA signaling. In addition, we show that TBC1D15 is required for the accumulation of RhoA at the equatorial cortex for the ingression of the cytokinetic furrow during cytokinesis. Our results demonstrate a novel role for TBC1D15 in the regulation of RhoA during membrane blebbing and cytokinesis.
AB - Membrane blebs are round-shaped dynamic membrane protrusions that occur under many physiological conditions. Membrane bleb production is primarily controlled by actin cytoskeletal rearrangements mediated by RhoA. Tre2-Bub2-Cdc16 (TBC) domain-containing proteins are negative regulators of the Rab family of small GTPases and contain a highly conserved TBC domain. In this report, we show that the expression of TBC1D15 is associated with the activity of RhoA and the production of membrane blebs. Depletion of TBC1D15 induced activation of RhoA and membrane blebbing, which was abolished by the addition of an inhibitor for RhoA signaling. In addition, we show that TBC1D15 is required for the accumulation of RhoA at the equatorial cortex for the ingression of the cytokinetic furrow during cytokinesis. Our results demonstrate a novel role for TBC1D15 in the regulation of RhoA during membrane blebbing and cytokinesis.
UR - https://www.scopus.com/pages/publications/84896544375
UR - https://www.scopus.com/pages/publications/84896544375#tab=citedBy
U2 - 10.1007/s11010-013-1921-2
DO - 10.1007/s11010-013-1921-2
M3 - Article
C2 - 24337944
AN - SCOPUS:84896544375
SN - 0300-8177
VL - 389
SP - 9
EP - 16
JO - Molecular and Cellular Biochemistry
JF - Molecular and Cellular Biochemistry
IS - 1-2
ER -