Homozygous pyd^B12 and transheterozygous pyd^B12/Df(3R)p-XT103 flies are adult viable, with slightly reduced zygotic viability (23-24% of progeny, as opposed to 33% expected). These zygotic mutant adults exhibit bristle defects and rough eyes.

Viability of the progeny of pyd^B12 homozygous mothers is strongly compromised, with mutant animals achieving adulthood at 1-23% of the expected number.

Maternal and zygotic pyd^B12 mutant embryos display 60% embryonic lethality. These embryos exhibit a set of cuticle defects consistent with a failure in head involution and minor defects in dorsal closure.

Maternal and zygotic pyd^B12 mutant embryos can assemble and maintain adherens junctions and assemble a leading edge actomyosin cable.

Substantial embryonic lethality (43-58%) is found in flies from pyd^ex147 mothers crossed with pyd^B12 fathers.

The ventral epidermis is intact in pyd^B12/pyd^ex147 maternal/zygotic mutant embryos and the CNS is not obviously hypertrophied. While approximately 17% of pyd^B12/pyd^ex147 maternal/zygotic mutant embryos appear wild-type, most mutant embryos (64%) exhibit defects in head involution that result in defective head skeletons, whereas the most severe (19%) display complete failure of head involution, leading to a hole in the cuticle. In addition, some show minor defects in dorsal closure.

Dorsal openings in embryos both maternally and zygotically mutant for pyd^B12 are often oval-shaped, as opposed to 'eye-shaped' as in wild-type. In some cases, failure of the head involution process results in zippering at the anterior canthus being prevented. In extreme cases, zippering at the posterior end seems largely or completely blocked, whereas in others it is simply slowed substantially. Although in most cases dorsal closure is eventually completed, cell shapes often remain quite irregular even when the two sheets meet, with small regions where the sheets do not seal still evident. In a subset of embryos, dorsal closure fails and amnioserosal apoptosis leaves a large hole on the dorsal surface.

Dorsal closure in maternal and zygotic pyd^B12 mutant embryos is significantly slower (>50%) than in wild-type embryos.

Maternal and zygotic pyd^B12 mutant embryos appear indistinguishable from wild-type through germband retraction. In a subset of mutants, all the cell shape changes associated with dorsal closure proceed in an essentially wild-type manner. However a substantial majority of mutant embryos exhibit defects in cell shape changes in the epidermis. By stage 13, some leading edge cells exhibit very narrow leading edges, suggestive of excess constriction of the leading edge actin cable, whereas in others the leading edge is broader, consistent with disruption of the leading edge actin cable. As closure proceeded, these cell shape defects became more widespread. The leading edge of the epidermis was often wavy, and leading edge cells varied from hyperconstricted to broadened at the leading edge. In addition, groups of cells in the lateral epidermis sometimes fail to change shape at all. These mutants are still able to assemble an actin cable at their leading edge at the onset of dorsal closure, despite defects in cell shape. Myosin is also assembled into the leading edge cable in maternal and zygotic pyd^B12 mutant embryo. The cable is maintained in many cells as closure proceeds and remains localised to the leading edge even in mutants in which the dorsal opening is highly abnormal in shape.

At the end of dorsal closure, pyd^B12 maternal/zygotic mutant embryos retain very deep segmental grooves, extending deep into the embryo both dorsally and ventrally. This defect can be seen as early as the onset of dorsal closure (at this stage wild-type groves have begun to become shallower) and still extend all the way to the leading edge. These grooves remain abnormally deep through to the end of closure, both in embryos in which closure goes to completion and in those in which it fails completely.

The ventral epidermis is intact in pyd^B12 maternal/zygotic mutant embryos and the CNS is not obviously hypertrophied. While approximately 8% of pyd^B12 maternal/zygotic mutant embryos apear wild-type, most mutant embryos (69%) exhibit defects in head involution that result in defective head skeltons, whereas the most severe (23%) display complete failure of head involution, leading to a hole in the cuticle. In addition, some show minor defects in dorsal closure.

Maternal and zygotic mutant progeny of mothers heteroallelic for pyd^B12 and Df(3R)p-XT103 die as embryos, in contrast to embryos zygotically mutant for pyd (pyd^B12 or Df(3R)p-XT103) but maternally wild-type, which are embryonic viable.

Substantial embryonic lethality (43-58%) is found in flies from pyd^ex147 or pyd^ex180 mothers crossed with pyd^B12 fathers.

Zygotic pyd^B12 mutants exhibit defects in tracheal development, such as dorsal branch fusion failures and ectopic fusions between neighbouring dorsal branches. Some dorsal branches in pyd^B12 mutant embruos have more than one terminal cell. Approximately 60% of zygotic pyd^B12 mutants have severe fusion defects. Elimination of maternal pyd^B12 further increases the frequency and severity of dorsal branch defects, with 100% of pyd^B12 maternal+zygotic mutant embryos exhibiting severe dorsal branch defects.

Embryos that are maternally and zygotically mutant for pyd^B12 exhibit highly convoluted trachea.

pyd[+]/pyd^B12 is an enhancer of abnormal cell shape phenotype of ena²³