title: Synergistic cooperation of Sall4 and Cyclin D1 in transcriptional repression.
abstract: 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.
authors: Institut für Humangenetik und Anthropologie, Universität Freiburg, Freiburg, Germany.
authors: Johann
authors: J
authors: Böhm
authors: Frank J
authors: FJ
authors: Kaiser
authors: Wiktor
authors: W
authors: Borozdin
authors: Reinhard
authors: R
authors: Depping
authors: Jürgen
authors: J
authors: Kohlhase
mesh_terms: D000818:Animals; D019556:COS Cells; D002467:Cell Nucleus / Q000378:metabolism; D002522:Chlorocebus aethiops; D056741:Cyclin D; D016213:Cyclins / Q000502:physiology*; D004268:DNA-Binding Proteins / Q000502:physiology*; D051379:Mice; D012097:Repressor Proteins / Q000502:physiology; D014157:Transcription Factors / Q000502:physiology*; D014158:Transcription, Genetic / Q000187:drug effects*
chemical_list: D056741:Cyclin D; D016213:Cyclins; D004268:DNA-Binding Proteins; D012097:Repressor Proteins; C509167:Sall4 protein, mouse; D014157:Transcription Factors