Synergistic cooperation of Sall4 and Cyclin D1 in transcriptional repression

Loss of function mutations in SALL4 cause Okihiro syndrome, an autosomal dominant disorder characterised by radial ray malformations associated with Duane anomaly. In zebrafish and mouse Sall4 interacts with TBX5 during limb and heart development and plays a crucial role for embryonic stem (ES) cell...

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Bibliographic Details
Published in:Biochemical and biophysical research communications 2007-05, Vol.356 (3), p.773-779
Main Authors: Böhm, Johann, Kaiser, Frank J., Borozdin, Wiktor, Depping, Reinhard, Kohlhase, Jürgen
Format: Article
Language:English
Subjects:
60 APPLIED LIFE SCIENCES
Animals
CELL CYCLE
Cell cycle regulation
Cell Nucleus - metabolism
Cercopithecus aethiops
COS Cells
Cyclin D
Cyclin D1
Cyclins - physiology
Danio rerio
DNA-Binding Proteins - physiology
GENE REGULATION
GENES
HEART
HETEROCHROMATIN
HYBRIDIZATION
LUCIFERASE
MALFORMATIONS
MICE
Nuclear localization
Okihiro syndrome
PHASE TRANSFORMATIONS
Repressor Proteins - physiology
SALL4
Transcription Factors - physiology
Transcription, Genetic - drug effects
Transcriptional activity
YEASTS
ZINC
Zinc finger
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Summary:Loss of function mutations in SALL4 cause Okihiro syndrome, an autosomal dominant disorder characterised by radial ray malformations associated with Duane anomaly. In zebrafish and mouse Sall4 interacts with TBX5 during limb and heart development and plays a crucial role for embryonic stem (ES) cell pluripotency. Here we report the nuclear interaction of murine Sall4 with Cyclin D1, one of the main regulators of G 1 to S phase transition in cell cycle, verified by yeast two-hybrid assay, co-immunoprecipitation and intracellular co-localisation. Furthermore, using luciferase reporter gene assays we demonstrate that Sall4 operates as a transcriptional repressor located to heterochromatin and that this activity is modulated by Cyclin D1.
ISSN:0006-291X
1090-2104
DOI:10.1016/j.bbrc.2007.03.050