PMID- 21752992
OWN - NLM
STAT- MEDLINE
DCOM- 20110912
LR  - 20211020
IS  - 1529-2401 (Electronic)
IS  - 0270-6474 (Print)
IS  - 0270-6474 (Linking)
VI  - 31
IP  - 28
DP  - 2011 Jul 13
TI  - Bcl11b/Ctip2 controls the differentiation of vomeronasal sensory neurons in mice.
PG  - 10159-73
LID - 10.1523/JNEUROSCI.1245-11.2011 [doi]
AB  - The transcription factor Bcl11b/Ctip2 plays critical roles in the development of 
      several systems and organs, including the immune system, CNS, skin, and teeth. 
      Here, we show that Bcl11b/Ctip2 is highly expressed in the developing vomeronasal 
      system in mice and is required for its proper development. Bcl11b/Ctip2 is 
      expressed in postmitotic vomeronasal sensory neurons (VSNs) in the vomeronasal 
      epithelium (VNE) as well as projection neurons and GABAergic interneurons in the 
      accessory olfactory bulb (AOB). In the absence of Bcl11b, these neurons are born 
      in the correct number, but VSNs selectively die by apoptosis. The critical role 
      of Bcl11b in vomeronasal system development is demonstrated by the abnormal 
      phenotypes of Bcl11b-deficient mice: disorganization of layer formation of the 
      AOB, impaired axonal projections of VSNs, a significant reduction in the 
      expression of vomeronasal receptor genes, and defective mature differentiation of 
      VSNs. VSNs can be classified into two major types of neurons, vomeronasal 1 
      receptor (V1r)/Galpha(i2)-positive and vomeronasal 2 receptor (V2r)/Galpha(o)-positive 
      VSNs. We found that all Galpha(i2)-positive cells coexpressed Galpha(o) during 
      embryogenesis. This coexpression is also observed in newly differentiated neurons 
      in the adult VNE. Interestingly, loss of Bcl11b function resulted in an increased 
      number of V1r/Galpha(i2)-type VSNs and a decreased number of V2r/Galpha(o)-type VSNs, 
      suggesting that Bcl11b regulates the fate choice between these two VSN types. 
      These results indicate that Bcl11b/Ctip2 is an essential regulator of the 
      differentiation and dichotomy of VSNs.
FAU - Enomoto, Takayuki
AU  - Enomoto T
AD  - Department of Bioengineering, Graduate School of Bioscience and Bioengineering, 
      Tokyo Institute of Technology, Yokohama 226-8501, Japan.
FAU - Ohmoto, Makoto
AU  - Ohmoto M
FAU - Iwata, Tetsuo
AU  - Iwata T
FAU - Uno, Ayako
AU  - Uno A
FAU - Saitou, Masato
AU  - Saitou M
FAU - Yamaguchi, Tatsuya
AU  - Yamaguchi T
FAU - Kominami, Ryo
AU  - Kominami R
FAU - Matsumoto, Ichiro
AU  - Matsumoto I
FAU - Hirota, Junji
AU  - Hirota J
LA  - eng
GR  - R03 DC011143/DC/NIDCD NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Neurosci
JT  - The Journal of neuroscience : the official journal of the Society for 
      Neuroscience
JID - 8102140
RN  - 0 (Bcl11b protein, mouse)
RN  - 0 (Repressor Proteins)
RN  - 0 (Tumor Suppressor Proteins)
RN  - 56-12-2 (gamma-Aminobutyric Acid)
SB  - IM
CIN - J Neurosci. 2011 Dec 7;31(49):17761-3. PMID: 22159092
MH  - Animals
MH  - Cell Differentiation/*physiology
MH  - Interneurons/metabolism
MH  - Mice
MH  - Mice, Knockout
MH  - Olfactory Bulb/cytology/metabolism
MH  - Repressor Proteins/*metabolism
MH  - Sensory Receptor Cells/*metabolism
MH  - Tumor Suppressor Proteins/*metabolism
MH  - Vomeronasal Organ/*cytology/*metabolism
MH  - gamma-Aminobutyric Acid/metabolism
PMC - PMC3394408
MID - NIHMS386165
EDAT- 2011/07/15 06:00
MHDA- 2011/09/13 06:00
PMCR- 2012/01/13
CRDT- 2011/07/15 06:00
PHST- 2011/07/15 06:00 [entrez]
PHST- 2011/07/15 06:00 [pubmed]
PHST- 2011/09/13 06:00 [medline]
PHST- 2012/01/13 00:00 [pmc-release]
AID - 31/28/10159 [pii]
AID - 3708345 [pii]
AID - 10.1523/JNEUROSCI.1245-11.2011 [doi]
PST - ppublish
SO  - J Neurosci. 2011 Jul 13;31(28):10159-73. doi: 10.1523/JNEUROSCI.1245-11.2011.