Embryos laid by amx1/Df(1)Exel9049 mutant females exhibit a strong neurogenic phenotype with a dramatic increase in the number of neurons and fail to hatch, resulting in female sterility.
Stage 8 embryos produced from homozygous amx1 mutant mothers contain an increased number of neuroblasts compared to wild type. More than 90% of embryos are neurogenic and ~10% have denticles.
Embryos from amx1/Df(1)10-70d females die and show the hypertrophy of the central nervous system characteristic of amx1/amx1 progeny.
Displays locomotor activity rhythm with an approximately 24h period.
Hyperplasia of replicating sensory precursors: due to an increased number of ectodermal cells being recruited as sensory precursor cells.
Increase in SMCs per cluster in embryos lacking the maternal product.
Variable embryonic neurogenic phenotype.
Most homozygotes are indistinguishable from wild-type, but some flies have smaller eyes than normal with disarranged facets, giving a rough eye phenotype.
Eyes slightly reduced, narrower below; trident pattern stronger than in lz. Studies by Shannon (FBrf0023892) show that amx1 progeny and many amx1/+ progeny of amx1 mothers are embryonic lethals. Ovaries and egg production of amx1 females normal. General disorganization of early embryo with amx1/+ progeny of amx1 mothers less extreme than amx1 progeny (FBrf0025447) amx1/+ daughters show 0.2% survival; amx1/Dp(1;1)lz-2 show considerably higher survival (FBrf0040181); Lethal embryos exhibit hypertrophy of central nervous system at the expense of epidermal tissue (FBrf0037306; FBrf0040185). Similarly peripheral nervous elements, the sensilla, exhibit increased numbers and abnormal morphology; cells diverted from epidermal to neurological pathway (FBrf0045357). Embryonic phenotype locally rescuable by injections of ooplasm from wild-type or pcxunspecified ova during preblastoderm stages (FBrf0040181; FBrf0042361). lz/amx1 is wild type. Mosaics in amx1/+ daughters of +/+ or amx1/+ females show that ventral tissues are sensitive to reduced amx+ activity; no clones of amx1 tissue found in cuticle of amx1/+ daughters of amx1 mothers (FBrf0041016). RK2.
amx1/Df(1)Exel9049 has female sterile phenotype, suppressible | partially by Hsap\TM2D3amx.1
amx1 has neurogenic phenotype | maternal effect | embryonic stage 8 phenotype, suppressible by Nicd.hs
amx1/Df(1)Exel9049 has female sterile phenotype, non-suppressible by Hsap\TM2D3P155L.amx
amx1 has neurogenic phenotype | maternal effect | embryonic stage 8 phenotype, non-suppressible by NGV.3.hs
amx1 has neurogenic phenotype | maternal effect | embryonic stage 8 phenotype, non-suppressible by NECN.GV.3.hs
Nicd.hs, amx1/amx[+] has partially lethal - majority live phenotype
Nicd.hs, amx1/amx[+] has majority die during embryonic stage phenotype
amx1/Df(1)Exel9049 has embryonic/larval neuron | increased number | maternal effect | embryonic stage phenotype, suppressible | partially by Hsap\TM2D3amx.1
amx1/Df(1)Exel9049 has embryonic/larval neuron | increased number | maternal effect | embryonic stage phenotype, non-suppressible by Hsap\TM2D3P155L.amx
The heat-shocked progeny from heterozygous amx1 females crossed to N3.hs.T:Scer\GAL4,T:Hsim\VP16 males hatch at a similar rate to wild type and are viable.
The heat-shocked progeny from heterozygous amx1 females crossed to NECN.3.hs.T:Scer\GAL4,T:Hsim\VP16 males hatch at a similar rate to wild type and are viable.
The heat-shocked progeny from heterozygous amx1 females crossed to Nicd.hs males hatch at a reduced rate compared to wild type and only around 50% reach adulthood.
The neurogenic phenotypes seen in stage 8 embryos when homozygous amx1 mutant females are crossed to N3.hs.T:Scer\GAL4,T:Hsim\VP16 males (heat-shocked before the first delamination round) are similar to those seen when amx1 females are crossed to wild type males.
The neurogenic phenotypes seen in stage 8 embryos when homozygous amx1 mutant females are crossed to NΔECD.hs.cUa males (heat-shocked before the first delamination round) are similar to those seen when amx1 females are crossed to wild type males.
Fewer neurogenic phenotypes are seen in stage 8 embryos when homozygous amx1 mutant females are crossed to Nicd.hs males (heat-shocked before the first delamination round) than when amx1 females are crossed to wild type males.
No effect on the faf eye phenotype.
The sterility of amx1/Df(1)Exel9049 mutant females and the neurogenic phenotype seen in the progeny (the embryos contain dramatically increased number of neurons and fail to hatch) is partially rescued by combination with Hsap\TM2D3amx.1 (some of the embryos show a complete rescue of the neurogenic phenotype and the hatching rate reaches almost 35%), whereas Hsap\TM2D3P155L.amx fails to improve the phenotypes.
amx1/Df(1)Exel9049 is rescued by amx+t3.325
amx1 is rescued by amxCTLD.MUT
amx1 is partially rescued by Scer\GAL4arm.PU/amxUAS.cMa
amx1 is not rescued by amxDRF.NRL
amx+t3.325 fully rescues the sterility of amx1/Df(1)Exel9049 mutant females and the neurogenic phenotype seen in the progeny (the embryos contain dramatically increased number of neurons and fail to hatch).
Expression of amxScer\UAS.cMa under the control of Scer\GAL4arm.PU partially rescues the neurogenic cuticle phenotypes seen in embryos derived from amx1 mutant females. Approximately 80% of embryos are neurogenic and ~40% have denticles.
