Cytologically normal.
Nucleotide substitution: A961C Nucleotide substitution: G1003A. Amino acid replacement: T321P. Amino acid replacement: E335K.
A13966036C
A961C
T321P | Orc2-PA
T321P
One of two nucleotide changes in mutant. Less likely of the two changes to cause phenotype.
G13966078A
G1003A
E335K | Orc2-PA
E335K
One of two nucleotide changes in mutant. Probable cause of phenotype.
Chorion gene amplification is depressed in Orc22 egg chambers.
Mutant eggs have defective chorions.
Orc22 females produce thin or no chorion.
eggs of homozygous females defective in late-deposited outer layers of endochorion; endochorionic material deficient. Late-gene expression as measured by mRNA or protein levels defective; deficiency in the level of chorion-gene amplification in follicle cells. Homozygous females weakly fertile; produce eggs with grossly defective chorions; thin, missing most appendages and permeable. All chorion proteins reduced in abundance; chorion gene amplification reduced to 10% wild-type level (Snyder et al., 1986). Heterozygotes with lethal alleles more extreme and sterile.
The chorion phenotype is rescued by Orc2+t7.5.
Nusslein-Volhard.
Ovaries derived from homozygous females show greatly reduced incorporation of BrdU compared to wild-type, and labeling is mosaic in intensity among the follicle cells.