PMID- 7698644
OWN - NLM
STAT- MEDLINE
DCOM- 19950502
LR  - 20220311
IS  - 0890-9369 (Print)
IS  - 0890-9369 (Linking)
VI  - 9
IP  - 5
DP  - 1995 Mar 1
TI  - The Drosophila tumor suppressor gene warts encodes a homolog of human myotonic 
      dystrophy kinase and is required for the control of cell shape and proliferation.
PG  - 534-46
AB  - Homozygous loss of the warts (wts) gene of Drosophila, caused by mitotic 
      recombination in somatic cells, leads to the formation of cell clones that are 
      fragmented, rounded, and greatly overgrown compared with normal controls. 
      Therefore, the gene is required for the control of the amount and direction of 
      cell proliferation as well as for normal morphogenesis. The absence of wts 
      function also results in apical hypertrophy of imaginal disc epithelial cells. 
      Secretion of cuticle over and between the domed apical surfaces of these cells 
      leads to a honeycomb-like structure and gives the superficial wart-like phenotype 
      of mitotic clones on the adult. One wts allele allows survival of homozygotes to 
      the late larval stage, and these larvae show extensive imaginal disc overgrowth. 
      Because of the excess growth and abnormalities of differentiation that follow 
      homozygous loss, we consider wts to be a tumor suppressor gene. The wts gene is 
      defined by the breakpoints of overlapping deficiencies in the right telomeric 
      region of chromosome 3, region 100A, and by lethal P-element insertions and 
      excisions. It encodes a protein kinase that is most similar to human myotonic 
      dystrophy kinase, the Neurospora cot-1 protein kinase, two cell-cycle regulated 
      kinases of yeast, and several putative kinases from plants. These proteins define 
      a new subfamily of protein kinases that are closely related to but distinct from 
      the cyclic AMP-dependent kinases. Although myotonic dystrophy is defined by a 
      neuromuscular disorder, it is sometimes associated with multiple pilomatrixomas, 
      which are otherwise rare epithelial tumors, and with other tumors including 
      neurofibromas and parathyroid adenomas. Our results raise the possibility that 
      homozygous loss of the myotonic dystrophy kinase may contribute to the 
      development of these tumors.
FAU - Justice, R W
AU  - Justice RW
AD  - Developmental Biology Center, University of California, Irvine 92717.
FAU - Zilian, O
AU  - Zilian O
FAU - Woods, D F
AU  - Woods DF
FAU - Noll, M
AU  - Noll M
FAU - Bryant, P J
AU  - Bryant PJ
LA  - eng
SI  - GENBANK/L39837
GR  - CA-09338/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Genes Dev
JT  - Genes & development
JID - 8711660
RN  - 0 (DMPK protein, human)
RN  - 0 (Drosophila Proteins)
RN  - EC 2.7.- (Protein Kinases)
RN  - EC 2.7.1.- (LATS1 protein, human)
RN  - EC 2.7.1.- (wts protein, Drosophila)
RN  - EC 2.7.11.1 (Myotonin-Protein Kinase)
RN  - EC 2.7.11.1 (Protein Serine-Threonine Kinases)
SB  - IM
GS  - wts
MH  - Amino Acid Sequence
MH  - Animals
MH  - Base Sequence
MH  - Cell Division/genetics
MH  - Cell Size/genetics
MH  - Cells, Cultured
MH  - Chromosome Mapping
MH  - Cloning, Molecular
MH  - Drosophila/*enzymology/genetics/growth & development
MH  - *Drosophila Proteins
MH  - Genes, Insect/*genetics/physiology
MH  - Genes, Tumor Suppressor/*genetics/physiology
MH  - Humans
MH  - Molecular Sequence Data
MH  - Mutagenesis
MH  - Myotonin-Protein Kinase
MH  - *Protein Kinases
MH  - Protein Serine-Threonine Kinases/chemistry/*genetics/physiology
MH  - Sequence Analysis, DNA
MH  - *Sequence Homology, Amino Acid
MH  - Transcription, Genetic/genetics
EDAT- 1995/03/01 00:00
MHDA- 1995/03/01 00:01
CRDT- 1995/03/01 00:00
PHST- 1995/03/01 00:00 [pubmed]
PHST- 1995/03/01 00:01 [medline]
PHST- 1995/03/01 00:00 [entrez]
AID - 10.1101/gad.9.5.534 [doi]
PST - ppublish
SO  - Genes Dev. 1995 Mar 1;9(5):534-46. doi: 10.1101/gad.9.5.534.