Duplication of the AIF gene. The 5' copy has a frameshifting base pair insertion in both exon 3 and exon 6. The 3' copy of AIF has a frameshifting base pair insertion in exon 3. A single FRT site, a w+mW.hs marker and a RS(I-CreI) site are present between the duplicated copies.
abnormal cell number | embryonic stage | maternal effect (with AIFT2)
Dp(2;2)AIFT52 mutant neuroblast clones (carrying both the AIFT52.5' and AIFT52.3' mutations) maintain a single neuroblast and consist of many neuronal progeny.
Homozygotes hatch, but larvae die within several days after egg laying (AEL); approximately half of the larvae are dead by 6 days AEL and by day 8 all the homozygotes have died. The mutant larvae are noticeably smaller than normal within hours after hatching. By day 4 AEL, the mutant larvae are at the 1st and 2nd instar stage (in contrast to wild type, where most larvae have reached the 3rd larval instar by this stage). No third instar larvae are recovered. Growth arrest at L1 of the mutant larvae is exacerbated under crowded culture conditions.
Homozygous embryos show reduced developmental programmed cell death than controls. The pattern of neuronal cells appears unperturbed in the mutant embryos, but extra cells are present in the ventral nerve cord (VNC) and Bolwig's organ. The number of cells in the VNC is normal in abdominal segment A1, but increases in a posterior manner in segments A2-A6 compared to wild type.
Homozygous Dp(2;2)AIFT52 animals (carrying both the AIFT52.5' and AIFT52.3' mutations) hatch, but larvae die within several days after egg laying (AEL); approximately half of the larvae are dead by 6 days AEL and by day 8 all the homozygotes have died. The mutant larvae are noticeably smaller than normal within hours after hatching. By day 4 AEL, the mutant larvae are at the 1st and 2nd instar stage (in contrast to wild type, where most larvae have reached the 3rd larval instar by this stage). No third instar larvae are recovered. Growth arrest at L1 of the mutant larvae is exacerbated under crowded culture conditions.
Homozygous Dp(2;2)AIFT52 embryos (carrying both the AIFT52.5' and AIFT52.3' mutations) show reduced developmental programmed cell death than controls. The pattern of neuronal cells appears unperturbed in the mutant embryos, but extra cells are present in the ventral nerve cord (VNC) and Bolwig's organ. The number of cells in the VNC is normal in abdominal segment A1, but increases in a posterior manner in segments A2-A6 compared to wild type.
AIFT52 is a suppressor | partially of abnormal neuroanatomy | somatic clone | larval stage phenotype of fzy5032
AIFT52 is a non-suppressor of increased cell death phenotype of Mmus\Gria1Lc.UAS, Scer\GAL4hs.2sev
AIFT52 is a suppressor | partially of neuroblast | somatic clone | larval stage phenotype of fzy5032
AIFT52 is a non-suppressor of eye phenotype of Mmus\Gria1Lc.UAS, Scer\GAL4hs.2sev
AIFT52 partially suppresses the larval neuroblast proliferation defects seen in fzy5032 mutant clones: the double mutant clones consistently contain more progeny than a fzy5032 single mutant clone, albeit the frequency of neuroblast-containing clones appears similar in both single and double mutant clones.
As in wild type, Dp(2;2)AIFT52 (which carries both the AIFT52.5' and AIFT52.3' mutations) partially suppresses the larval neuroblast proliferation defects seen in fzy5032 mutant clones. The frequency of neuroblast-containing clones is similar with or without Dp(2;2)AIFT52.