Insert stated as cause: blood{}
Insert stated as cause: blood{} Point mutation.
One copy of abo1 weakly suppresses position effect variegation (PEV) at the w locus caused by In(1)wm4.
One copy of abo1 is unable to suppress the telomeric position effect (TPE) in stocks carrying a variegating P{hsp26-pt-T}39C-5 insertion at the telomere of the left arm of chromosome two.
Homozygous mothers produce embryos with two distinct lethal phenotypes: arrest at a stage before nuclear cycle 6 (unfertilised eggs) or predominantly embryos complete blastoderm formation, form cuticle but most fail to hatch. Mutant embryos show a range of cuticular defects, others die as larvae. Maternal effect lethality can be partially rescued by paternally derived abo+ and by increasing the dosage of specific regions of Y heterochromatin designated ABO. The phenocritical period for zygotic rescue by heterochromatin is late in embryogenesis after cuticle deposition but before hatching.
Lines constructed carrying this allele and differing in their genetic background (details not described) can be grouped into three classes. Complete reversion occurs only when the complete blood transposon is lost and after this event the mutant phenotype cannot reappear in subsequent generations. Partial reversion may take place without the complete loss of the transposon. Reappearance of the full abo phenotype can only take place in heterozygous lines constructed from partially revertant abo homozygous lines that have not lost the blood transposon.
Females produce defective eggs.
Probability of survival of embryos produced by abo1/abo1 mothers reduced; male embryos more severely affected than female embryos. Both preblastoderm and postblastoderm embryonic death observed; partial rescue of postblastoderm mortality effected by paternally inherited abo+ allele; partial rescue of preblastoderm mortality by heterochromatic ABO elements located in Xh between 3/4 and 7/8 of the distance from the centromere, in YL region h10-11, in YS region h19, in 2R proximal and perhaps in other heterochromatic regions (Pimpinelli, Sullivan, Prout and Sandler, 1985). Gradual loss of phenotype in homozygous abo stocks accompanied by increase in quantity of ribosomal DNA (Krider and Levine, 1975). New restriction fragments appear in HindIII/HaeIII double digests of such homozygous lines probed with nontranscribed spacer sequences of ribosomal genes (Graziani, Vicari, Boncinelli, Malva, Manzi, and Mariani, 1981). abo phenotype returns with subsequent maintenance in heterozygous condition.
abo1 has female sterile phenotype, suppressible by Df(2L)DS6
abo1 has female sterile phenotype, suppressible by Df(2L)DS9
abo1 has female sterile phenotype, suppressible by Df(2L)DS5
Isolated from: Near Rome, Italy population.
Preliminary experiments using a P-element-borne copy of the wild type Gyc32E 12kb genomic region failed to rescue either abo1 or l(2)gd11 phenotypes.
"FBti0014253 == Doc{}abo1" was stated as revision.
Frequency of nondisjunction in abo1/subDub is double that of subDub/+, however no increase in nondisjunction is observed in abo2/sub females, suggesting that the interaction of subDub with abo1 is allele specific or due to a locus elsewhere on the chromosome.
"FBti0014253 == Doc{}abo1" was stated as revision. Recessive fertilisation defect is either allele specific or due to a closely linked second mutation.