One copy of bic¹ is unable to suppress position effect variegation (PEV) at the w locus caused by In(1)w^m4.

One copy of bic¹ 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.

bic¹/Df(2R)vg-B hemizygous females produce some bicaudal (13.2% of unhatched embryos) and headless embryos.

bic¹/Df(2R)vg-B females produce embryos with anterior duplications (symmetrical and asymmetrical) of posterior segments.

Homozygous females produce variable numbers of eggs that fail to hatch (e.g., 25-50%). bic¹/Df(2R)vg-B females produce higher embryonic mortality. Males of either genotype are normal. A wide array of developmental anomalies observed among arrested embryos. Many fail to show outward signs of initiation of development, although in at least some zygotes nuclear divisions can be demonstrated. Others show replacement of anterior embryonic segments by a mirror-image set of posterior segments. The majority of these bicaudal embryos are symmetrical with opposing sets of the two to five posterior-most segments; mirror-imaged structures include denticle belts, posterior spiracles, Malpighian tubules, genital disc and posterior midgut invagination. Pole cells form at the original but not the duplicated posterior end. Asymmetrical bicaudal embryos such as 3/6 or 3/7 have fewer duplicated than original posterior segments. Other embryos have the head replaced by posterior abdominal structures or show abnormal development of the cephalopharyngeal apparatus. Finally, some embryos are foreshortened and seem to lack internal segments. Maximum production of bicaudal embryos occurs in the first eggs produced by females developing at 28^oC-29^oC. The incidence of bicaudal embryos falls rapidly during the first 60 hr after eclosion. Incidence of bicaudal embryos and nondeveloping eggs depends on genotype: bic¹/Df(2R)vg-B > bic¹/Df(2R)vg-D > Df(2R)vg-B/+ > bic¹/bic¹ > bic¹/+ = 0.