embryonic/first instar larval cuticle & embryonic head | germ-line clone
eye (with Su(H)2), with Scer\GAL4da.PU, Su(H)UAS.GFP,Tag:V5
eye disc & neuron | somatic clone | cell autonomous
proneural cluster & dorsal mesothoracic disc
wing (with Su(H)2), with Scer\GAL4da.PU, Su(H)UAS.GFP,Tag:V5
When expression is driven using Scer\GAL4da.PU, Su(H)Scer\UAS.T:Avic\GFP,T:SV5\V5 rescues viability of Su(H)2/Su(H)8, although adult flies have some wing and eye defects (reminiscent of reduced N function).
Homozygotes are lethal during pupal development.
Heterozygous flies carrying out 10 training sessions to test memory of odours display a lower 24 hour memory in spaced training (rest periods between tasks) compared to control flies.
No difference in 24 hour memory is seen in heterozygotes carrying out massed training (no rest period) compared to controls.
Heterozygotes tested immediately and 3 hours after one training session did not show any difference in memory from wild type.
No unusual cell death is observed in wing pouch clones.
Mitotic clones of cells carrying Su(H)8 grow normally at any position within the eye disc.
Homozygous follicle cell clones are smaller than surrounding wild-type cells and the mutant cells undergo additional mitoses.
Wing primordium is established but does not grow. Lateral inhibition fails in the notum, causing an excess of neural precursors.
Homozygous clones do not reliably disrupt the dorsal/ventral boundary in the wing disc.
The number of ftz expressing MP2 neurons increases compared to wild-type (About 15 on each side of the midline, as compared to 2 in wild-type) in homozygous embryos derived from homozygous female germ-line clones (lacking both maternal and zygotic function). In homozygous embryos derived from homozygous female germ-line clones (lacking both maternal and zygotic function), RP2sib neurons become eve expressing RP2 neurons. Usib neurons also appear to become U neurons.
Mutant embryos develop a larger patch of dorsal cuticle than that developed by corresponding N mutants.
Many cells in clones induced in the central domain of the ZNC in the developing wing enter S phase. Those in anterior clones located next to wg expressing cells arrest in G2.
Homozygous clones in the eye imaginal disc show autonomous neural hypertrophy. Many of these ectopic neural cells are R8 photoreceptors.
The number of cells in the nau-expressing muscle precursor clusters is wild-type in homozygous embryos. The number of cells in the nau-expressing muscle precursor clusters is increased compared to wild-type in homozygous embryos derived from homozygous female germline clones (lacking both maternal and zygotic function). The number of cells in the nau-expressing muscle precursor clusters is increased compared to wild-type in homozygous DlM2 embryos. The severity of the phenotype is not altered if the embryos are also homozygous for Su(H)8.
Mutation suppresses the hair cell to socket cell transformation, but not the neuron to sheath cell transformation. Homozygous clones in the IIa cell due to Scer\FLP1Scer\UAS.cBa expression driven by Scer\GAL4sca-537.4 or Scer\GAL4sca-109-68 cause a twinned hair phenotype.
Su(H)8/Su(H)IB115 wings are reduced to stumps.
Homozygous embryos derived from germ-line clones exhibit a strong neurogenic cuticular phenotype and fail to hatch. The number of neuroblasts and sensory precursors that segregate from the ventral and dorsolateral neuroectoderm, respectively, is greatly increased. This leads to hypertrophy of the CNS and PNS and failure of ventral and head cuticle to develop. No defect is seen in the nervous system when rescued by wild type paternal copy of Su(H). Heterozygous embryos derived from germ-line clones survive to adulthood.
Cells within homozygous clones located at wild type sensory organ positions adopt the sensory organ precursor (SOP) fate, even when directly juxtaposed to wild type cells. Su(H) mutant SOPs express a neuronal fate.
Mosaic analysis reveals two bristle phenotypes. When recombination is induced in the first and second larval instar patches of naked cuticle result. Recombination later results in double-shaft bristles.
Lethality during the first day of pupal development. Supernumerary cells stained in mutant imaginal discs have adopted a sensory organ precursor (SOP) fate instead of the epidermal fate they would normally express. The excess SOPs arise from the proneural clusters of potential precursor cels that appear in the imaginal discs during the development of wild type bristles. The wing pouch region of the wing imaginal disc and the retinal field of the eye-antennal imaginal disc are dramatically reduced. Identical phenotype is seen when transheterozygous with Df(2L)TE35BC-24, Su(H)1, Su(H)2 or Su(H)IB115.
Su(H)8 has lethal | recessive | larval stage phenotype, suppressible by Tom8
Su(H)8/Su(H)[+] is an enhancer of visible | adult stage phenotype of Scer\GAL4sca-109-68, hamUAS.cMa
Su(H)8/Su(H)2 is a non-enhancer of visible phenotype of NECNΔ10-12.UAS, Scer\GAL4ptc-559.1
Su(H)8 is a non-suppressor of increased cell death | somatic clone phenotype of l(2)gd1d7
Su(H)8/Su(H)2 is a non-suppressor of visible phenotype of NECNΔ10-12.UAS, Scer\GAL4ptc-559.1
Su(H)8, Tom[+]/Tom8 has lethal | recessive | pupal stage phenotype
Su(H)8/Su(H)2 has proneural cluster phenotype, suppressible by Scer\GAL4klu-G410/E(spl)m8-HLHUAS.cNa
Su(H)8/Su(H)2 has proneural cluster phenotype, suppressible by E(spl)m7-HLHUAS.cdCa/Scer\GAL4klu-G410
Su(H)8 has eye-antennal disc phenotype, suppressible by Tom8
Su(H)8/Su(H)2 has wing phenotype, suppressible by Scer\GAL4ptc-559.1/vgUAS.cKa
Su(H)8/Su(H)2 has wing phenotype, suppressible by Scer\GAL4dpp.blk1/vgUAS.cKa
Su(H)8/Su(H)2 has wing disc phenotype, non-suppressible by DeltaUAS.cHa/Scer\GAL4dpp.blk1
Su(H)8/Su(H)2 has wing disc phenotype, non-suppressible by Scer\GAL4klu-G410/E(spl)m8-HLHUAS.cNa
Su(H)8/Su(H)2 has wing disc phenotype, non-suppressible by E(spl)m7-HLHUAS.cdCa/Scer\GAL4klu-G410
Su(H)8/Su(H)2 has wing disc phenotype, non-suppressible by Nint.SH.UAS/Scer\GAL4dpp.blk1
Su(H)8/Su(H)2 has wing disc phenotype, non-suppressible by Scer\GAL4dpp.blk1/SerUAS.cSa/vgUAS.cKa
Su(H)8/Su(H)2 has wing phenotype, non-suppressible by wgUAS.cGa/Scer\GAL4dpp.blk1
Su(H)8/Su(H)[+] is an enhancer of notal microchaeta | adult stage phenotype of Scer\GAL4sca-109-68, hamUAS.cMa
Su(H)8/Su(H)[+] is an enhancer of tormogen cell | adult stage phenotype of Scer\GAL4sca-109-68, hamUAS.cMa
Su(H)8/Su(H)[+] is an enhancer of trichogen cell | adult stage | ectopic phenotype of Scer\GAL4sca-109-68, hamUAS.cMa
Su(H)8 is a suppressor of mechanosensory sensory organ phenotype of Hsap\APLP2::Hsap\APPUAS.Tag:MYC, Scer\GAL4sca-537.4
Su(H)8 is a suppressor of adult head phenotype of Tom8
Su(H)8/Su(H)[+] is a suppressor of phenotype of Src42ASu(Raf)1-1
Su(H)8 is a suppressor of trichogen cell phenotype of numb2
Su(H)8 is a suppressor of trichogen cell phenotype of numbSW
Su(H)8/Su(H)del47 is a non-suppressor of wing disc phenotype of aprK568/apUGO35
Sox154AA, Su(H)8/Su(H)2, Su(H)RC-ΔASE has tormogen cell phenotype
Scer\GAL4dpp.blk1, Su(H)8, vgUAS.cKa has wing phenotype
Scer\GAL4ptc-559.1, Su(H)8, vgUAS.cKa has wing phenotype
Su(H)2 Sox154AA/Su(H)8 Sox154AA; Su(H)RC-ΔASE mutants show a more dramatic socket differentiation defect than either single mutant. Most of the double mutant bristles have a convex (rather than concave) socket-shaft cuticular interface. Dome of these bulbous socket structures extend one or more small cuticular projections, while others extend one or two distinctly shaft-like structures.
The neurogenic phenotype, but not the wing development phenotype, of Su(H)2/Su(H)8 is strongly suppressed by either HLHm7Scer\UAS.cdCa or E(spl)Scer\UAS.cNa driven by Scer\GAL4klu-G410. The wing development phenotype of Su(H)2/Su(H)8 is not suppressed by either Nint.SH.Scer\UAS or DlScer\UAS.cHa, or SerScer\UAS.cSa in combination with vgScer\UAS.cKa, driven by Scer\GAL4dpp.blk1. The wing development phenotype of Su(H)2/Su(H)8 is also not suppressed by HE31.
Partially suppresses the Tom8 phenotype - Su(H)8/+ ; Tom8/Tom8 pharate adults show almost completely everted head structures. The larval lethality and small eye-antennal disc phenotype of Su(H)8 homozygotes can be partially rescued by Tom8 - Su(H)8/Su(H)8 ; Tom8/+ animals develop to the pupal stage with pharate adults showing partially everted heads.
The addition of Su(H)2/Su(H)8 has no effect on the proneural cluster phenotype in the wing disc seen in NECNΔ10-12.Scer\UAS/Scer\GAL4ptc-559.1 discs. Expression of Ncdc10.Scer\UAS.T:Hsap\MYC driven by Scer\GAL4ptc-559.1 has no effect on the Su(H)8/Su(H)2 proneural cluster phenotype in the wing disc.
Does not enhance the wing nicking phenotype seen in mamN.Scer\UAS, Scer\GAL4C96 flies.
Dominantly suppresses the ability of Src42ASu(phl)1-1 to suppress the lethality of phl1/Y flies.
Scer\GAL4dpp.blk1-mediated or Scer\GAL4ptc-559.1-mediated expression of vgScer\UAS.cKa substantially rescues the wing blade phenotype. Scer\GAL4dpp.blk1-mediated expression of wgScer\UAS.cGa does not rescue loss of wing tissue.
Su(H)8/Su(H)2 is rescued by Su(H)UAS.GFP,Tag:V5/Scer\GAL4da.PU
Su(H)8 is rescued by Su(H)hs.PS
Su(H)8 is rescued by Su(H)UAS.cPa/Scer\GAL4Mef2.247
Su(H)8/Su(H)2 is rescued by Su(H)+t6.0
Su(H)8/Su(H)2 is partially rescued by Scer\GAL4klu-G410/Su(H)UAS.cKa
Su(H)8/Su(H)2 is partially rescued by Scer\GAL4dpp.blk1/Su(H)UAS.cKa
Su(H)8 is not rescued by Su(H)UAS.cPa/Scer\GAL4Alp4-c232
When expression is driven using Scer\GAL4da.PU, Su(H)Scer\UAS.T:Avic\GFP,T:SV5\V5 rescues viability of Su(H)2/Su(H)8.
Expression of Su(H)hs.PS with 30 minutes heat shock at 37C rescues the reduced 24 hour memory phenotype seen in Su(H)8 homozygotes.
When expression of Su(H)Scer\UAS.cKa is driven by Scer\GAL4dpp.blk1 in a Su(H)2/Su(H)8 mutant the wing pouch size defect is rescued. When expression of Su(H)Scer\UAS.cKa is driven by Scer\GAL4klu-G410 in a Su(H)2/Su(H)8 mutant the neurogenesis and wing pouch size defects are rescued.
Ashburner.
Double mutant analysis fails to establish a strict epistatic relationship between H and Su(H) for the specification of sensory organ precursor fate.