PMID- 15946822
OWN - NLM
STAT- MEDLINE
DCOM- 20050926
LR  - 20200106
IS  - 0736-5748 (Print)
IS  - 0736-5748 (Linking)
VI  - 23
IP  - 5
DP  - 2005 Aug
TI  - Spatial and temporal localization during embryonic and fetal human development of 
      the transcription factor SIM2 in brain regions altered in Down syndrome.
PG  - 475-84
AB  - Human SIM2 is the ortholog of Drosophila single-minded (sim), a master regulator 
      of neurogenesis and transcriptional factor controlling midline cell fate 
      determination. We previously localized SIM2 in a chromosome 21 critical region 
      for Down syndrome (DS). Here, we studied SIM2 gene using a new approach to 
      provide insights in understanding of its potential role in human development. For 
      the first time, we showed SIM2 spatial and temporal expression pattern during 
      human central nervous system (CNS) development, from embryonic to fetal stages. 
      Additional investigations were performed using a new optic microscopy technology 
      to compare signal intensity and cell density [M. Rachidi, C. Lopes, S. Gassanova, 
      P.M. Sinet, M. Vekemans, T. Attie, A.L. Delezoide, J.M. Delabar, Regional and 
      cellular specificity of the expression of TPRD, the tetratricopeptide Down 
      syndrome gene, during human embryonic development, Mech. Dev. 93 (2000) 
      189--193]. In embryonic stages, SIM2 was identified predominantly in restricted 
      regions of CNS, in ventral part of D1/D2 diencephalic neuroepithelium, along the 
      neural tube and in a few cell subsets of dorsal root ganglia. In fetal stages, 
      SIM2 showed differential expression in pyramidal and granular cell layers of 
      hippocampal formation, in cortical cells and in cerebellar external granular and 
      Purkinje cell layers. SIM2 expression in embryonic and fetal brain could suggest 
      a potential role in human CNS development, in agreement with Drosophila and mouse 
      Sim mutant phenotypes and with the conservation of the Sim function in CNS 
      development from Drosophila to Human. SIM2 expression in human fetal brain 
      regions, which correspond to key structures for cognitive processes, correlates 
      well with the behavioral phenotypes of Drosophila Sim mutants and transgenic mice 
      overexpressing Sim2. In addition, SIM2-expressing brain regions correspond to the 
      altered structures in DS patients. All together, these findings suggest a 
      potential role of SIM2 in CNS development and indicate that SIM2 overexpression 
      could participate to the pathogenesis of mental retardation in Down syndrome 
      patients.
FAU - Rachidi, Mohammed
AU  - Rachidi M
AD  - EA 3508, Tour 54, E2-54-53, Case 7104, Universite Denis Diderot, 2 Place Jussieu, 
      75251 Paris, France. mrachidi@9online.fr
FAU - Lopes, Carmela
AU  - Lopes C
FAU - Charron, Giselle
AU  - Charron G
FAU - Delezoide, Anne-Lise
AU  - Delezoide AL
FAU - Paly, Evelyne
AU  - Paly E
FAU - Bloch, Bernard
AU  - Bloch B
FAU - Delabar, Jean-Maurice
AU  - Delabar JM
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Int J Dev Neurosci
JT  - International journal of developmental neuroscience : the official journal of the 
      International Society for Developmental Neuroscience
JID - 8401784
RN  - 0 (Basic Helix-Loop-Helix Transcription Factors)
RN  - 0 (SIM2 protein, human)
RN  - 0 (Transcription Factors)
SB  - IM
MH  - Basic Helix-Loop-Helix Transcription Factors
MH  - Brain/*embryology
MH  - Down Syndrome/*embryology
MH  - Embryo, Mammalian/metabolism
MH  - Fetus/metabolism
MH  - Gestational Age
MH  - Humans
MH  - Time Factors
MH  - Tissue Distribution
MH  - Transcription Factors/*metabolism
EDAT- 2005/06/11 09:00
MHDA- 2005/09/27 09:00
CRDT- 2005/06/11 09:00
PHST- 2005/01/04 00:00 [received]
PHST- 2005/03/14 00:00 [revised]
PHST- 2005/05/03 00:00 [accepted]
PHST- 2005/06/11 09:00 [pubmed]
PHST- 2005/09/27 09:00 [medline]
PHST- 2005/06/11 09:00 [entrez]
AID - S0736-5748(05)00063-8 [pii]
AID - 10.1016/j.ijdevneu.2005.05.004 [doi]
PST - ppublish
SO  - Int J Dev Neurosci. 2005 Aug;23(5):475-84. doi: 10.1016/j.ijdevneu.2005.05.004.