There is a delay in neuronal determination of photoreceptor cell precursor clusters in homozygous clones in the eye disc compared to the adjacent wild-type clusters. The developing photoreceptor cell preclusters show defects in cell arrangement and occasionally cell number, with defects first seem at the five cell precluster stage. The cluster sometimes does not rotate properly. R3/R3 type symmetrical ommatidia (where the R3 or R4 cell has not taken up the correct position) are found at the borders of homozygous clones in the eye. In these ommatidia, either the R3 or R4 cell, or both, is mutant and the chirality of these ommatidia is sometimes also incorrect. Homozygous clones in the eye result in a scar. The scar contains no photoreceptor cells but pigment cells are still present. The photoreceptor cells have developed, but have fallen out of the retinal epithelium onto the lamina of the optic lobe of the brain and the basal fenestrated membrane of the retina. Mutant cells in larval eye discs show depletion or more diffuse localisation of F-actin, especially in the more posterior part of the mutant clone. Mosaic ommatidia have a lower concentration of F-actin in their photoreceptor cells than normal and it is found more basally than in the wild-type neighbouring cells.
Mutant embryos do not retract their germband during stage 13. In mutants embryos the early aspects of tracheal cell fate specification and morphogenesis are indistinguishable from wild-type. During stages 14 and 15, mutant embryos exhibit several tracheal defects, foremost of which is the constriction and expansion of the dorsal trunk to form sac-like structures. Similar defects are seen in the smaller tracheal branches which collapse and become misshapen. By stage 16 many sacs have pinched off and tubes no longer connect these sacs. the lumen is no longer continuous and secondary branching does not occur. Tracheal defects are most severe in the posterior region of the embryo. The tracheal epithelium in pebhnt-1 mutant embryos has ultrastructurally normal zonula adherentes that are present apicolaterally as in wild-type. Regions of the trachea are either collapsed or expanded compared with wild-type and in places the lumen is severely reduced in size. There are no obvious defects in either the polarity or the general cytological organisation of the surviving tracheal cells in pebhnt-1 mutants either prior to or during loss of normal epithelial architecture. In pebhnt-1 mutant trachae the epicuticle is secreted but there are no taenidial folds in either the collapsed or the expanded regions.
Genetic mosaic embryos show phenotypes that reveal a correlation between the genotype of the amnioserosa and the success or failure of germ band retraction. 100% of mosaics where germband retraction was successful had peb+ tissue in the amnioserosa. 100% of embryos with a fully mutant amnioserosa failed to undergo germ band retraction. The genotype of the anterior or posterior midgut is not correlated with the success or failure of germ band retraction. Analysis of distribution of mutant cells in mosaic amnioserosa suggests that peb function is important in those amnioserosa cells that abut the epidermis.
79% of embryos have abdominal segment 5.0 +/- 0.5 at the posterior tip, indicating a failure of germband retraction.
Homozygous embryos exhibit weak germ band retraction defects. Kr staining reveals abnormalities in the amnioserosa.
Germband retraction and dorsal closure fail to occur in homozygous embryos.
Nondefective in gonad assembly.
Within constraints of the embryo being folded due to the hnt mutation, the muscle pattern is normal and movement is vigorous and well coordinated.
The germ band does not retract in pebhnt-1 embryos. Embryos are U-shaped with the head facing posteriorly.
embryonic lethal no germ band retraction; embryo U-shaped with head facing posteriorly. Germ line clones obtained; no maternal effect in homozygous germ-line clones (Perrimon, Engstrom, and Mahowald, 1989).
pebhnt-1 has mitotic domain 1 | extended germ band stage phenotype, suppressible by InRhs.PF
pebhnt-1 has embryo | dorsal closure stage phenotype, suppressible by InRhs.PF
pebhnt-1 has amnioserosa phenotype, non-suppressible by InRhs.PF
Df(3L)H99, pebhnt-1 has embryonic/larval tracheal system phenotype
The failure of germband retraction can be rescued by pebhs.PY.
l(1)EH275a is not allelic to peb; l(1)EH275a1 complements pebhnt-1, pebX001, pebEH704a and peb1.