PMID- 26702832
OWN - NLM
STAT- MEDLINE
DCOM- 20160513
LR  - 20211203
IS  - 1878-1551 (Electronic)
IS  - 1534-5807 (Print)
IS  - 1534-5807 (Linking)
VI  - 35
IP  - 6
DP  - 2015 Dec 21
TI  - Fat/Dachsous Signaling Promotes Drosophila Wing Growth by Regulating the 
      Conformational State of the NDR Kinase Warts.
PG  - 737-49
LID - S1534-5807(15)00762-5 [pii]
LID - 10.1016/j.devcel.2015.11.027 [doi]
AB  - Nuclear Dbf2-related (NDR) kinases play a central role in limiting growth in most 
      animals. Signals that promote growth do so in part by suppressing the activation 
      of NDR kinases by STE20/Hippo kinases. Here, we identify another mechanism for 
      downregulating NDR kinase activity. Specifically, we show that activity of the 
      Drosophila NDR kinase Warts in the developing wing depends on its transition from 
      an inactive, "closed" conformation to a potentially active, "open" conformation 
      mediated by Mats, a conserved Mps1-binder (Mob) protein. Further, we show that 
      signaling interactions between the protocadherins Fat and Dachsous, organized by 
      the morphogens Wingless and Decapentaplegic, suppress Warts by acting via the 
      atypical myosin Dachs to inhibit or reverse this transition. The regulation of 
      Warts conformation by Mats, Fat/Dachsous signaling, and Dachs appears independent 
      of Warts phosphorylation by Hippo kinase, establishing a precedent for the 
      control of NDR kinases, and hence growth, by distinct allosteric and 
      phosphorylation mechanisms.
CI  - Copyright (c) 2015 Elsevier Inc. All rights reserved.
FAU - Vrabioiu, Alina M
AU  - Vrabioiu AM
AD  - Department of Genetics and Development, Columbia University College of Physicians 
      and Surgeons, New York, NY 10032, USA.
FAU - Struhl, Gary
AU  - Struhl G
AD  - Department of Genetics and Development, Columbia University College of Physicians 
      and Surgeons, New York, NY 10032, USA. Electronic address: gs20@columbia.edu.
LA  - eng
GR  - R01 GM109183/GM/NIGMS NIH HHS/United States
GR  - R01 GM113000/GM/NIGMS NIH HHS/United States
GR  - Howard Hughes Medical Institute/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Dev Cell
JT  - Developmental cell
JID - 101120028
RN  - 0 (Cadherins)
RN  - 0 (Cell Adhesion Molecules)
RN  - 0 (Drosophila Proteins)
RN  - 0 (ds protein, Drosophila)
RN  - 0 (ft protein, Drosophila)
RN  - EC 2.7.1.- (trc protein, Drosophila)
RN  - EC 2.7.11.1 (Protein Serine-Threonine Kinases)
SB  - IM
CIN - Dev Cell. 2015 Dec 21;35(6):666-8. PMID: 26702824
MH  - Animals
MH  - Cadherins/metabolism
MH  - Cell Adhesion Molecules/metabolism
MH  - Drosophila Proteins/*metabolism
MH  - Drosophila melanogaster/genetics/growth & development/*metabolism
MH  - Protein Serine-Threonine Kinases/*metabolism
MH  - *Signal Transduction
MH  - Wings, Animal/*growth & development
PMC - PMC4709125
MID - NIHMS741500
EDAT- 2015/12/26 06:00
MHDA- 2016/05/14 06:00
PMCR- 2016/12/21
CRDT- 2015/12/26 06:00
PHST- 2015/06/19 00:00 [received]
PHST- 2015/09/01 00:00 [revised]
PHST- 2015/11/25 00:00 [accepted]
PHST- 2015/12/26 06:00 [entrez]
PHST- 2015/12/26 06:00 [pubmed]
PHST- 2016/05/14 06:00 [medline]
PHST- 2016/12/21 00:00 [pmc-release]
AID - S1534-5807(15)00762-5 [pii]
AID - 10.1016/j.devcel.2015.11.027 [doi]
PST - ppublish
SO  - Dev Cell. 2015 Dec 21;35(6):737-49. doi: 10.1016/j.devcel.2015.11.027.