Imprecise excision of P{SUPor-P}KG02994 has deleted genomic sequence from the insertion site to codon 303 of Nc (in exon 2).
Nc51 mutant eye clones exhibit extra ommatidial pigment cells in the pupal retina.
S2PKG08356/S2P1, Nc51/+ and S2PKG08356/S2P1, Nc51/Nc51 mutant larvae exhibit lethality between second and third instar stages. Lethality is rescued partially by supplementing fly food with fatty acids, but viability is still reduced compared to S2PKG08356/S2P1 mutants.
Nc51 mosaic wings retain Disc\RFPhs.DsRedT4.T:nls5-positive wing epithelial cells 4-11 days after eclosion, whereas control epithelial cells undergo apoptosis moments after eclosion.
Wing blemishes are not seen in Nc51 heterozygotes.
Programmed cell death inCrz-expressing neurons in the ventral nerve cord is significantly delayed in Nc51/NcI24 mutants. Approximately 12 neurons still survive at 7 hours after pupal formation, while the number is reduced to approximately 8 at 16 hours after pupal formation, and none at 48 hours after pupal formation.
Nc51/NcI29 mutants exhibit a delay in programmed cell death in Crz-expressing neurons in the ventral nerve cord during pupation.
Dendrites of Nc51 mutant C4da neuron clones appear normal at larval stages. However, unlike wild-type, these neurons fail to properly prune their larval dendrites during metamorphosis and most display relatively intact primary and secondary larval dendritic arbors at 18 hours after puparium formation.
Nc51 homozygous embryos hatch at the normal time, but the larvae develop more slowly than wild-type. These larvae fail to pupariate, but continue to grow for some time after controls pupariate. The resulting giant larvae die at 10-12 days after wild-type larvae pupariate. Unlike wild-type larvae, these larvae are not induced to pupariate early by feeding with ecdysone at the mid-third instar.
Nc51 homozygous larvae fail to exhibit cell death in the larval midgut ,as wild-type larvae do, at end of the third larval instar (assayed by Tunel staining) or in response to feeding with ecdysone at mid-third instar (assayed by acridine orange staining).
Nc51 homozygous embryos display head involution defects. Post-embryonic growth of these animals is slower than in wild-type and both larval moults and pupation are delayed. However, once they do reach the wandering late third instar larval stage, these larvae are generally bigger wild-type counterparts and have larger and sometimes deformed discs and brain. They also exhibit hyperplasia of the blood cells. These animals die during early pupal stages, sometimes with visible melanotic tumors.
Nc51 homozygous embryos laid by NcKG02994/Nc51 mothers do not hatch and have more severe head involution defects than Nc51 homozygotes laid by wild-type mothers. These have embryos decreased levels of cell death, as assayed by tunel staining, in the epidermis at stage 12 and the ventral nerve cord at stage 15/16. Consistent with a reduction in cell death, increases in cell number are see in multiple cases: Extra cells are associated with Bolwig's organ at stage 15 and extra cells are present in the ventral nerve cord at late embryonic stages
NcKG02994/Nc51 adults have a higher frequency of post-alar bristle duplication than NcKG02994 homozygous adults.
Adult eyes completely populated by Nc51 homozygous somatic clone cells are normal sized but rough. This is not due to supernumerary photoreceptor cells, however, ommatidial pre-clusters are irregularly spaced immediately posterior to the furrow in late third instar eye discs of this genotype.
No obvious defects are present in the wings of newly eclosed flies carrying Nc51 homozygous clones. But, the wings of these flies develop melanized blotches as they age.
Cultured hemocytes isolated from third instar Nc51 homozygous larvae are much less sensitive to induction of apoptosis by a variety of pro-apoptotic agents (cycloheximide, Actinomycin D, etoposide (Topoisomerase II inhibitor), ethanol, and smac mimetic) than wild-type controls. In addition, levels of constitutive apoptosis in these cells are significantly lower than controls.
DroncI24/Dronc51 has abnormal cell death phenotype, enhanceable by Strica4
DroncI24/Dronc51 has abnormal cell death phenotype, suppressible by DreddL23
Dronc51 is an enhancer of abnormal neuroanatomy phenotype of Scer\GAL4insc-Mz1407, numbS2D.UAS
Dronc51/Dronc[+] is a suppressor | partially of decreased size | adult stage phenotype of Scer\GAL4nub.PU, sydGLC01419
Dronc51/Dronc[+] is a suppressor | partially of visible | adult stage phenotype of Scer\GAL4nub.PU, sydGLC01419
Dronc51/Nc[+] is a suppressor of abnormal neurophysiology phenotype of ninaE17, ninaEP37H
Dronc51/Nc[+] is a suppressor of abnormal neuroanatomy phenotype of ninaE17, ninaEP37H
Dronc51/Nc[+] is a suppressor of viable | conditional phenotype of S2PKG08356/S2P1
Dronc51/Dronc51 is a suppressor of viable | conditional phenotype of S2PKG08356/S2P1
Dronc51 is a non-suppressor of abnormal neuroanatomy | larval stage phenotype of fzy1/fzy5032
Dronc51 is a non-suppressor of decreased cell number | larval stage phenotype of fzy1/fzy5032
Dronc51 is an enhancer of neuroblast phenotype of Scer\GAL4insc-Mz1407, numbS2D.UAS
Dronc51 is an enhancer of type II neuroblast | increased number phenotype of Scer\GAL4insc-Mz1407, numbS2D.UAS
Dronc51/Nc[+] is a suppressor of rhabdomere of eye photoreceptor cell phenotype of ninaE17, ninaEP37H
Dronc51/Nc[+] is a suppressor of eye phenotype of grimGMR.PH
Dronc51 is a non-suppressor of neuroblast | larval stage phenotype of fzy1/fzy5032
A Nc51 heterozygous background enhances ectopic neuroblast formation due to numbS2D.Scer\UAS expression.
Nc51/+ partially suppresses the small, rough eye phenotype caused by rprGMR.PH or grimGMR.PH but not that caused by WGMR.PG.
Dronc51 is partially rescued by DroncUAS.EGFP/Scer\GAL4hs.PB
Dronc51 is partially rescued by Dronc+t.drf
Dronc51 is not rescued by DroncC318S.UAS/Scer\GAL4hs.PB
Associated with: CG668551