Open AccessDeletion mapping in the Enhancer of split complex
Author(s) -
Wurmbach Elisa,
Preiss Anette
Publication year - 2014
Publication title -
hereditas
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.819
H-Index - 50
eISSN - 1601-5223
pISSN - 0018-0661
DOI - 10.1111/hrd2.00065
Subject(s) - biology , enhancer , gene , genetics , phenotype , repressor , effector , notch signaling pathway , mutant , mutagenesis , basic helix loop helix , microbiology and biotechnology , dna binding protein , transcription factor
The Enhancer of split complex [E(spl)‐C] comprises twelve genes of different classes. Seven genes encode proteins of with a basic‐helix‐loop‐helix‐orange (bHLH‐O) domain that function as transcriptional repressors and serve as effectors of the Notch signalling pathway. They have been named E(spl)m8‐, m7‐, m5‐, m3‐, mβ‐, mγ‐ and mδ‐HLH . Four genes, E(spl)m6‐, m4‐, m2‐ and mα‐BFM are intermingled and encode Notch repressor proteins of the Bearded‐family (BFM). The complex is split by a single gene of unrelated function, encoding a Kazal‐type protease inhibitor ( Kaz‐m1 ). All members within a family, bHLH‐O or BFM, are very similar in structure and in function. In an attempt to generate specific mutants, we have mobilised P‐element constructs residing next to E(spl)m7‐HLH and E(spl)mγ‐HLH , respectively. The resulting deletions were mapped molecularly and by cytology. Two small deletions affected only E(spl)m7‐HLH and E(spl)mδ . The deficient flies were viable without apparent phenotype. Larger deletions, generated also by X‐ray mutagenesis, uncover most of the E(spl)‐C . The phenotypes of homozygous deficient embryos were analysed to characterize the respective loss of Notch signalling activity.