Polytene chromosomes normal.
Val replaced for a Asp.
Amino acid replacement: V?E. V?E falls in the HLH domain.
T783A. This changes a valine located at the end of Helix 1 into an aspartic acid.
Point mutation.
T749812A
T783A
V50D | emc-PA
V?D
wing | somatic clone (with Df(3L)emc-E12)
somatic clones of emc1 cells in the ovarian follicle cells look morphologically normal during most of oogenesis. However, the resulting egg chamber often have dorsal appendage defects. These defects take a variety of forms, from split-ends through varying degress of fusion, to almost complete loss. Follicle cell imprints on the shells of these eggs show that at least some main body follicle cells are abnormally large and/or misshapen.
Homozygous follicle cell clones can result in fused egg chambers containing 32 germline nuclei. These egg chambers contain 2 oocyte nuclei suggesting that they probably result from fusion of two distinct cysts. These fused egg chambers have polar cells only at the termini of the fused cysts.
emc1/Df(3L)emc-E12 cells do not form normal size clones in the wing. Homozygous clones in the wing show ectopic veins in specific positions and only occasionally cause the differentiation of thicker veins.
emc1/emc11 flies have slightly smaller wings than normal, although the wing vein pattern is normal. emc1 clones in rhove-1 vn1 wings differentiate as veins in positions possibly corresponding to those of wild-type veins. Vein differentiation in these clones frequently fails in distal regions of veins. emc1 clones in bs2 wings differentiate as vein everywhere in the wing blade covering intervein regions as vein. The ectopic wing vein phenotype of px72 wings is exaggerated in regions occupied by emc1 homozygous clones. The borders of the emc1 clones respect not only normal veins as restriction borders, but also tend not to cross ectopic veins. Clones in the wing intervein regions that are doubly mutant for Gap1B1 and emc1 largely differentiate as veins. Clones in the wing intervein regions that are doubly mutant for rhoWk and emc1 largely differentiate as veins.
Extra neuron mutant.
emc1/Df(3L)emc-E12 clones in the wing show defects in cell proliferation but overall wing size is not affected due to compensation by growth of surrounding non-mutant cells. Clones are very elongated and preferentially appear along the veins and wing margin. Clones can differentiate veins but exhibit an emc phenotype. Homozygous clones in the wing also exhibit proliferation defects causing a reduction in wing size. Clones can shift the position of veins and fuse veins but reducing the intervein region. Homozygous and hemizygous clones in the notum, leg and haltere cause similar defects, shortening of segments and deletion of structures.
Variations in chaetae number and size: ectopic macrochaetae and mesochaetae appear as a second and third posterior row, microchaetae smaller than wild type differentiate posteriorly to the macrochaetae.
Extra chaetae form in characteristic patterns.
very strong, although not amorphic phenotype.
homozygous lethal
emc1 has visible | somatic clone phenotype, enhanceable by DeltaM1/Dl[+]
emc1 has visible | somatic clone phenotype, enhanceable by N[+]/N55e11
emc1 has visible | somatic clone phenotype, enhanceable by Nl1N-ts1/N[+]
emc1 has visible | somatic clone phenotype, non-enhanceable by N[+]/NAx-M3
emc1 has visible | somatic clone phenotype, non-suppressible by N[+]/NAx-M3
emc1 has wing vein | somatic clone phenotype, enhanceable by DeltaM1/Dl[+]
emc1 has wing vein | somatic clone phenotype, enhanceable by N[+]/N55e11
emc1 has wing vein | somatic clone phenotype, enhanceable by Nl1N-ts1/N[+]
emc1 has wing vein | somatic clone phenotype, non-enhanceable by N[+]/NAx-M3
emc1 has macrochaeta | ectopic | somatic clone phenotype, non-suppressible by NMcd1
emc1/Df(3L)emc-E12 has phenotype, non-suppressible | somatic clone by NAx-M3/NAx-M3
emc1/Df(3L)emc-E12 has wing | somatic clone phenotype, non-suppressible by NAx-M3/NAx-M3
emc1 has wing vein | somatic clone phenotype, non-suppressible by N[+]/NAx-M3
emc1/emc11 is a suppressor of wing vein L4 phenotype of Egfrf37/Egfrt1
emc1/emc11 is a suppressor of wing vein L4 phenotype of vnddd-3/vn1
emc1/Df(3L)emc-E12, N55e11 has wing phenotype
emc1/Df(3L)emc-E12, N55e11 has wing | somatic clone phenotype
emc1, hry22 has eye disc morphogenetic furrow phenotype
Clones of N55e11/N55e11; emc1/Df(3L)emc-E12 cells in the wing have extremely poor viability. The failure of emc1/Df(3L)emc-E12 cells to form normal size clones in the wing is not rescued if the flies are also homozygous for NAx-M3. The width of wing veins formed by clones of homozygous emc1 cells is increased if the flies are also heterozygous for N55e11 or DlM1 but is unaffected if the flies are heterozygous for NAx-M3. Homozygous emc1 clones induced in a Nl1N-ts1/+ background result in thickening of the wing veins when pupal development takes place at 29oC (the restrictive temperature for the Nl1N-ts1 allele).
emc1/emc11 suppresses the loss of wing vein L4 seen in vn1/vnddd-3 or Egfrt1/Egfrf37 flies. The interactions between emc1/emc11 and rhove-1/rhove-1 or rhove-1/rho9 are additive. The ectopic wing vein phenotype of EgfrE3/+ flies is slightly enhanced by emc1/emc11. The ectopic wing vein phenotype of rhoStg/rhoWk flies is slightly enhanced by emc1/emc11. The extra wing vein phenotype of px72 homozygotes is enhanced by emc1/+ or emc1/emc11. The extra wing vein phenotype of net1 homozygotes is enhanced by emc1/+. net1/+ ; emc1/emc11 flies show an extra wing vein phenotype. The extra wing vein phenotype of bs2 homozygotes is enhanced by emc1/emc11. bs03267/+ ; emc1/emc11 flies show an extra wing vein phenotype.
Ripoll.
Phenotypes of emc alleles can be ordered, going from weakest to strongest: emc1 < emc1/Df(3L)emc-E12 < emc9 = emcip15 = emc9/emcip15 < emc9/Df(3L)emc-E12 = emcip15/Df(3L)emc-E12 < Df(3L)emc-E12/Df(3L)emc-E12.