PMID- 20512118
OWN - NLM
STAT- MEDLINE
DCOM- 20100909
LR  - 20231113
IS  - 1476-4687 (Electronic)
IS  - 0028-0836 (Print)
IS  - 0028-0836 (Linking)
VI  - 466
IP  - 7305
DP  - 2010 Jul 22
TI  - Phenotypic robustness conferred by apparently redundant transcriptional 
      enhancers.
PG  - 490-3
LID - 10.1038/nature09158 [doi]
AB  - Genes include cis-regulatory regions that contain transcriptional enhancers. 
      Recent reports have shown that developmental genes often possess multiple 
      discrete enhancer modules that drive transcription in similar spatio-temporal 
      patterns: primary enhancers located near the basal promoter and secondary, or 
      'shadow', enhancers located at more remote positions. It has been proposed that 
      the seemingly redundant activity of primary and secondary enhancers contributes 
      to phenotypic robustness. We tested this hypothesis by generating a deficiency 
      that removes two newly discovered enhancers of shavenbaby (svb, a transcript of 
      the ovo locus), a gene encoding a transcription factor that directs development 
      of Drosophila larval trichomes. At optimal temperatures for embryonic 
      development, this deficiency causes minor defects in trichome patterning. In 
      embryos that develop at both low and high extreme temperatures, however, absence 
      of these secondary enhancers leads to extensive loss of trichomes. These 
      temperature-dependent defects can be rescued by a transgene carrying a secondary 
      enhancer driving transcription of the svb cDNA. Finally, removal of one copy of 
      wingless, a gene required for normal trichome patterning, causes a similar loss 
      of trichomes only in flies lacking the secondary enhancers. These results support 
      the hypothesis that secondary enhancers contribute to phenotypic robustness in 
      the face of environmental and genetic variability.
FAU - Frankel, Nicolas
AU  - Frankel N
AD  - Howard Hughes Medical Institute and Department of Ecology and Evolutionary 
      Biology, Princeton University, Princeton, New Jersey 08544, USA.
FAU - Davis, Gregory K
AU  - Davis GK
FAU - Vargas, Diego
AU  - Vargas D
FAU - Wang, Shu
AU  - Wang S
FAU - Payre, Francois
AU  - Payre F
FAU - Stern, David L
AU  - Stern DL
LA  - eng
GR  - R01 GM063622/GM/NIGMS NIH HHS/United States
GR  - R01 GM063622-09/GM/NIGMS NIH HHS/United States
GR  - HHMI/Howard Hughes Medical Institute/United States
GR  - GM063622-06A1/GM/NIGMS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
DEP - 20100530
PL  - England
TA  - Nature
JT  - Nature
JID - 0410462
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (Drosophila Proteins)
RN  - 0 (Transcription Factors)
RN  - 0 (ovo protein, Drosophila)
SB  - IM
CIN - Nat Rev Genet. 2010 Jul;11(7):454. PMID: 20548292
MH  - Animal Structures/anatomy & histology/embryology
MH  - Animals
MH  - DNA-Binding Proteins/*genetics
MH  - Drosophila Proteins/*genetics
MH  - Drosophila melanogaster/anatomy & histology/*embryology/*genetics/growth & 
      development
MH  - Enhancer Elements, Genetic/*genetics
MH  - *Gene Expression Regulation, Developmental
MH  - Larva/anatomy & histology/genetics/growth & development
MH  - Models, Genetic
MH  - *Phenotype
MH  - Temperature
MH  - Transcription Factors/*genetics
MH  - Transcription, Genetic/*genetics
MH  - Transgenes/genetics
PMC - PMC2909378
MID - NIHMS204229
EDAT- 2010/06/01 06:00
MHDA- 2010/09/10 06:00
PMCR- 2011/01/01
CRDT- 2010/06/01 06:00
PHST- 2009/12/30 00:00 [received]
PHST- 2010/05/11 00:00 [accepted]
PHST- 2010/06/01 06:00 [entrez]
PHST- 2010/06/01 06:00 [pubmed]
PHST- 2010/09/10 06:00 [medline]
PHST- 2011/01/01 00:00 [pmc-release]
AID - nature09158 [pii]
AID - 10.1038/nature09158 [doi]
PST - ppublish
SO  - Nature. 2010 Jul 22;466(7305):490-3. doi: 10.1038/nature09158. Epub 2010 May 30.