Transient, heat-shock induced expression of Nint.hs inhibits photoreceptor differentiation in a band of cells in the developing eye disc.
Nint.hs inhibits sensory organ precursor cell formation in wing discs.
NΔECN.hs blocks SOP formation in wild type and nct mutant wing discs.
Expression of Nint.hs at 34-35oC at 128-132 hours after egg laying (AEL) often results in ectopic veinlets running from the posterior crossvein through the inner distal intervein area. There are additional vein spots near L5. Expression of Nint.hs at 34-35oC at 140-144 hours AEL results in ectopic vein spots between L4 and L5 and ectopic cross veins. Expression of Nint.hs at 34-35oC at 152-156 hours AEL results in the distal parts of the longitudinal veins being missing while ectopic veins are formed in the proximal regions of the wing.
Expression of Nint.hs using heat shock results in a band of cells where ommatidium differentiation is blocked posterior to the morphogenetic furrow. These cells enter the second mitotic wave but do not divide (accumulating in G2).
Heat shock during embryonic stages 9 and 10 reduces the size of the mushroom bodies, due to prevention of mushroom body neuroblast delamination.
When heatshocked, mutant embryos develop without Malpighian tubule tip cells. This phenotype is seen whether expression is driven from 5 hours after egg laying, or from 6 or 7 hours after egg laying.
Flies in which Nint.hs has been expressed using heat shock during the larval stage show some absence of neural development in the ommatidia. In addition, symmetrical ommatidia with the shape expected for ommatidia containing two R4 photoreceptor cells are seen.
After heatshocking Nint.hs embryos, both progeny from the GMC4-2a ganglion mother cell appear to adopt the RP2sib neuronal fate. After heatshocking, both progeny from the GMC1-1a ganglion mother cell appear to adopt the pCC neuronal fate.
Expression of this constitutively active form of N during the division of GMC-1 into RP2 or sib, leads to the specification of sib fate to both progeny.
Heat induced expression transforms pIIb into a second pIIa: sensory organs form composed of two shaft and two socket cells. Cell fate transformation is not sufficient to change the orientation of cell division of ectopic pIIa.
At 25oC causes no effect on wing vein formation and the adult wing is wild type. When induced with 2 hour heat pulses at 37oC initiated at times from 22 to 32 hours APF, vein loss is observed, being most extreme with a heat pulse between 26 and 28 hours APF. Flies show shortening of L2, L4, L5 and some shortening of L3.
Heat induced expression from 13 to 15 hours after puparium formation (APF) causes most macrochaetae organs to develop as double-sockets and loss of microchaetae. Expression from 18 to 20 hours APF causes microchaetae composed of twin shafts associated with sockets (correlated with absence of neurons). Expression from 22 to 24 hours causes development of double socket microchaetae and loss of the trichogen cell. Deformed shafts are seen after expression from 30 to 32 hours APF. Many macrochaetae shafts exhibit deformed shafts following expression from 18 to 32 hours.
Results in the absence of olfactory sense organs when expressed between 0 and 25 hours after puparium formation.
Suppresses the effects of dshhs.PA in the wing.
A single pulse of expression causes a gap of about four columns lacking any photoreceptor differentiation.
Invagination and delamination of SNSPs is blocked. Heat pulses between 5hrs and 7hrs of embryogenesis prevented invagination of the three SNS pouches. Later pulses block the separation of the SNS pouches from the esophageal epithelium. Differentiation of SNS neurons is substantially delayed.
Expression induces wing outgrowth.
Strong 'microchaetae loss' phenotype. At macrochaetae positions shafts are lost and extra sockets are present (shaft to socket cell transformation).
90 minute heat shock at 7hrs APF leads to a highly penetrant loss of microchaetae. Sensillum precursors are missing. In combination with Hhs.PB, pattern of bristles closely resembles wild type.
Clones in the wing pouch cause outgrowth.
Expression during the larval/pupal stages produces H--like phenotypes. Expression during the third larval instar causes selective loss of macrochaetae on the notum and head. Expression during 0-24hr APF results in double socket sensilla at all or most macrochaetae and microchaetae sites on head or notum of adults. The double socket phenotype results from a tormogen to trichogen transformation. Nint.hs causes other H--like phenotypes in the wing margin, wing veins and interommatidial bristles.
Behaves as a gain of function mutation, even in the absence of endogenous Notch activity, and has its effect when cell fate decisions are being made. In embryos and in imaginal discs, neuroblast segregations are suppressed and all ectodermal cells give rise to epidermis. The product of this allele becomes nuclear-localized.