745 bp deletion removing the ATG translation start site, the first and second exons, and 18 bp of the third exon. A 7.9kb cassette carrying a w+* marker replaces the deleted sequence.
745 bp region at the 5' end of eater (which includes the ATG translation start site, the first and second exons, and 18 bp of the third exon) was deleted by homologous recombination and replaced with a 7.9kb cassette carrying the w gene.
eater1 homozygotes raised on poor diet exhibit partial lethality during P-stage.
Flies carrying the eater1 lesion are viable and appear developmentally wild type.
eater1 larval hemocytes show defects in phagocytosis of Gram-positive but not Gram-negative bacteria.
Sessile plasmatocytes are absent or almost absent in eater1 mutant larvae. Dissected eater1 mutant larvae release more than three times the number of hemocytes than wild-type, indicating an abnormally high number of hemocytes in circulation. The lymph glands of eater1 mutant larvae are not visibly different in size to those of wild-type. The sessile plasmatocyte striped pattern evident in wild-type larvae is absent in eater1 mutants. All or almost all plasmatocytes in the mutant larvae are in circulation and appear not to enter the sessile state. This 'no sessile plasmatocyte' phenotype is phenocopied in trans-heterozygous larvae carrying eater1 over the deficiencies Df(3R)Exel6206 and Df(3R)BSC791.
Clonal analysis of eater1 mutant hemocytes indicates that the sessile plasmatocyte defect is a cell-autonomous phenotype.
Compared with wild-type, eater1 mutant plasmatocytes show a reduction in cell area on a glass substrate, indicating defects in adhesion.
Sessile crystal cells are absent or almost absent in eater1 mutant larvae.
NimC11, eater1 has embryonic/larval hemocyte | increased number | larval stage phenotype
NimC11, eater1 has embryonic/larval plasmatocyte | larval stage phenotype