The mob as tumor suppressor gene is essential for early development and regulates tissue growth in Drosophila

Takeshi Shimizu, Li Lun Ho, Zhi Chun Lai

Research output: Contribution to journalArticle

25 Citations (Scopus)

Abstract

Studies in Drosophila have defined a new growth inhibitory pathway mediated by Fat (Ft), Merlin (Mer), Expanded (Ex), Hippo (Hpo), Salvador (Sav)/Shar-pei, Warts (Wts)/Large tumor suppressor (Lats), and Mob as tumor suppressor (Mats), which are all evolutionarily conserved in vertebrate animals. We previously found that the Mob family protein Mats functions as a coactivator of Wts kinase. Here we show that mats is essential for early development and is required for proper chromosomal segregation in developing embryos. Mats is expressed at low levels ubiquitously, which is consistent with the role of Mats as a general growth regulator. Like mammalian Mats, Drosophila Mats colocalizes with Wts/Lats kinase and cyclin E proteins at the centrosome. This raises the possibility that Mats may function together with Wts/Lats to regulate cyclin E activity in the centrosome for mitotic control. While Hpo/Wts signaling has been implicated in the control of cyclin E and diap1 expression, we found that it also modulates the expression of cyclin A and cyclin B. Although mats depletion leads to aberrant mitoses, this does not seem to be due to compromised mitotic spindle checkpoint function.

Original languageEnglish (US)
Pages (from-to)957-965
Number of pages9
JournalGenetics
Volume178
Issue number2
DOIs
StatePublished - Feb 1 2008

Fingerprint

Warts
Tumor Suppressor Genes
Drosophila
Cyclin E
Growth
Centrosome
Phosphotransferases
Neurofibromin 2
M Phase Cell Cycle Checkpoints
Cyclin B
Cyclin A
Mitosis
Vertebrates
Neoplasms
Proteins
Embryonic Structures
Fats

All Science Journal Classification (ASJC) codes

  • Genetics

Cite this

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The mob as tumor suppressor gene is essential for early development and regulates tissue growth in Drosophila. / Shimizu, Takeshi; Ho, Li Lun; Lai, Zhi Chun.

In: Genetics, Vol. 178, No. 2, 01.02.2008, p. 957-965.

Research output: Contribution to journalArticle

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