Reference Report

Reference
Citation	Ligoxygakis, P., Bray, S.J., Apidianakis, Y., Delidakis, C. (1999). Ectopic expression of individual E(spl) genes has differential effects on different cell fate decisions and underscores the biphasic requirement for notch activity in wing margin establishment in Drosophila. Development 126(10): 2205--2214. (Export to RIS)
FlyBase ID	FBrf0108430
Publication Type	Research paper
PubMed ID	10207145
PubMed Abstract	A common consequence of Notch signalling in Drosophila is the transcriptional activation of seven Enhancer of split [E(spl)] genes, which encode a family of closely related basic-helix-loop-helix transcriptional repressors. Different E(spl) proteins can functionally substitute for each other, hampering loss-of-function genetic analysis and raising the question of whether any specialization exists within the family. We expressed each individual E(spl) gene using the GAL4-UAS system in order to analyse their effect in a number of cell fate decisions taking place in the wing imaginal disk. We focussed on sensory organ precursor determination, wing vein determination and wing pattern formation. All of the E(spl) proteins affect the first two processes in the same way, namely they antagonize neural precursor and vein fates. Yet, the efficacy of this antagonism is quite distinct: E(spl)mbeta has the strongest vein suppression effect, whereas E(spl)m8 and E(spl)m7 are the most active bristle suppressors. During wing patterning, Notch activity orchestrates a complex sequence of events that define the dorsoventral boundary of the wing. We have discerned two phases within this process based on the sensitivity of N loss-of-function phenotypes to concomitant expression of E(spl) genes. E(spl) proteins are initially involved in repression of the vg quadrant enhancer, whereas later they appear to relay the Notch signal that triggers activation of cut expression. Of the seven proteins, E(spl)mgamma is most active in both of these processes. In conclusion, E(spl) proteins have partially redundant functions, yet they have evolved distinct preferences in implementing different cell fate decisions, which closely match their individual normal expression patterns.
DOI
Related Publication(s)
Recent Updates
Description	What does this section display? This section contains items that were added to this record for each release. It currently only tracks new links between this FlyBase report and other FlyBase data classes (e.g. genes, references, stocks) or controlled vocabulary terms (e.g. GO, anatomy terms). What does this section not display? This section does not currently display links that were removed or gene model changes.
Update Feed	Click the icon below to subscribe to this FlyBase record and receive updates automatically through your feed reader.
FB2013_03
FB2013_02
All updates	Click here to see a list of all updates to this record from FB2010_08 and on.
Associated Information
Comments
Associated Files
Other Information
Secondary IDs
Language of Publication	English
Additional Languages of Abstract
Also Published As
Parent Publication
Publication Type	Journal
Abbreviation	Development
Title	Development
Publication Year	1987-
ISBN/ISSN	0950-1991
Data from Reference
Aberrations (2)
	Df(1)N-54l9 Df(3R)gro^b32.2
Alleles (21)
	E(spl)m3-HLH^Scer\UAS.cLa E(spl)m5-HLH^Scer\UAS.cLa E(spl)m7-HLH^{Scer\UAS.cdCa} E(spl)m8-HLH^Scer\UAS.cNa E(spl)mβ-HLH^{Scer\UAS.cdCa} E(spl)mγ-HLH^Scer\UAS.cLa E(spl)mδ-HLH^{Scer\UAS.cdCa} Ecol\lacZ^{E(spl).-1166+87} Ecol\lacZ^Scer\UAS.cUa Ecol\lacZ^vg.806 Ecol\lacZ^vg.int2.1 Ecol\lacZ^wg-en11 gro^E48 N^l1N-ts1 N^nd-3 Scer\GAL4^32B Scer\GAL4^455.2 Scer\GAL4^ap-md544 Scer\GAL4^bi-omb-Gal4 Scer\GAL4^h-1J3 w^+mC
Constructs (11)
	P{m8-lacZ} P{UAS-E(spl).N} P{UAS-E(spl)mβ} P{UAS-HLHm3.L} P{UAS-HLHm5.L} P{UAS-HLHm7.C} P{UAS-HLHmγ.L} P{UAS-lacZ.U} P{UAS-mδ} P{vg(806)-lacZ} P{vg(D/V)-lacZ}
Genes (15)
	ct Dll E(spl)m3-HLH E(spl)m5-HLH E(spl)m7-HLH E(spl)m8-HLH E(spl)mβ-HLH E(spl)mγ-HLH E(spl)mδ-HLH Ecol\lacZ gro N Scer\GAL4 w wg
Insertions (6)
	P{en1}wg^en11 P{GAL4}bi^omb-Gal4 P{GawB}32B P{GawB}455.2 P{GawB}ap^md544 P{GawB}h^1J3