hkb^gurt/hkb² embryos show the visceral mesoderm defects seen in hkb^gurt embryos.

Stage 15-16 hkb² embryos have strong defects in the visceral muscle.

Glia are absent from the CNS of hkb² mutant embryos.

Mutant embryos have abnormal salivary glands; 3% have elongated, branched lumens, 30% have elongated, expanded lumens and 67% have short, narrow lumens (normal salivary glands have elongated, unbranched lumens). Mutant salivary gland cells have reduced apical areas at all stages of salivary gland formation. Constriction of the apical domain is not as coordinated in invaginating mutant cells as in wild-type cells and occurs over a wider region of the salivary gland placode than normal. Once internalised, the mutant cells do not expand their apical domains to the same extent as wild-type cells and many of the mutant internalised cells do not polarise in the proximal-distal direction (in contrast to wild type). In hkb² embryos, the cells in the centre of the salivary gland placode are the first to invaginate, in contrast to wild type, where the dorsal-posterior cells invaginate first. The dorsal-posterior cells of the placode do not invaginate in mutant embryos. Mutant salivary gland cells show ultrastructural abnormalities at the apical surface once they begin to invaginate; they have less microvilli at the apical surface and less apical membrane than wild-type cells. The apical domains of the internalised mutant cells also appear disorganised; the distance between the apex of the cell and the adherens junctions is greater than normal.

The salivary gland placodes of hkb² embryos appear identical to wild type. The first gross morphological defect seen is the incorrect positioning of the site of internalisation; the first cells to invaginate are those in the middle of the placode (in contrast to wild type where the first cells to invaginate are in the dorsal-posterior region of the placode). The invaginating pit is a mixture of wedge-shaped cells with constricted apices and basal nuclei, and elongated cells with randomly positioned nuclei (in wild-type all invaginating cells are approximately the same length and are wedge-shaped with basal nuclei). The pit is wider and shallower than in wild type and appears to include more cells. The invaginating salivary glands are trapezoidal shaped. The order of invagination is disrupted; cells immediately surrounding the pits appear to change shape and invaginate simultaneously. All secretory cells are eventually internalised, but the salivary glands are positioned more anteriorly and lie closer to the ventral midline and the body wall than the salivary glands of wild-type embryos. The characteristic cigar-shaped tubes of wild-type salivary glands are never formed, but the mutant salivary glands fuse along the ventral midline, forming dome-shaped organs with a commen lumen. Once invagination of the secretory cells is complete, open pits remain, as in wild-type embryos.

Most of the ectopic serotonergic cells and most of the wild-type serotonergic cells found in larvae derived from embryos expressing eg^Scer\UAS.cDa under the control of Scer\GAL4^sca-537.4 are missing if the larvae are also homozygous for hkb².

hkb² tll¹ double mutant embryos show twisted gastrulation. hkb² tld⁹ double mutant embryos undergo germband extension, but fail to undergo germband retraction.

The aCC and pCC neurons are normal in homozygotes, but interneurons of the neuroblast (NB) 1-1 lineage lie in an abnormally ventral position and have pathfinding defects, often having abnormal contralateral projections. The ipsilateral interneurons sometimes project anteriorly or in multiple longitudinal fascicles. The motoneuron which normally projects from the segmental nerve (SN) in the thorax either has no projection, a projection that terminates prematurely in the SN, or a projection into the anterior root of the intersegmental nerve. A large cell of unknown origin is sometimes seen close to the aCC and pCC neurons. All glial cells in the abdomen derived from NB 1-1 are missing, and appear to be replaced by extra neuronal cells. NB 2-2 produces the normal number, position and type of cells in homozygous embryos, but the interneurons and motoneurons derived from it show pathfinding defects; the interneuronal projections in the thorax often have small ectopic ispilateral extensions and the contralateral bundle is loosely fasciculated. The motoneurons in the thorax often leave the central nervous system (CNS) through the wrong fascicle and terminate just outside the CNS before reaching their target muscles. Abdominal interneurons and motoneurons of the NB 2-2 lineage also have pathfinding defects.

Intermediate hkb allele.

Oesophagus, stomatogastric nervous system, labral nerve, epiphysis, dorsopharyngeal organ and pharyngeal monoscolopidial chordotonal organ are deleted.

No effect on prd expression in embryo.

In hkb² tll^g double mutant embryos the posterior border of gt stripe 4 retracts even less than in tll^g mutants.

Does not interact with RpII140^wimp maternal effect.

Failure of head involution. Absence of anterior midgut. In 50% of embryos a small remnant of posterior midgut is present, in 50% there is no posterior midgut at all.

hkb²/hkb[+] is a suppressor | partially of chaeta | increased number phenotype of gcm^Pyx

hkb² is a suppressor of serotonergic neuron | ectopic phenotype of Scer\GAL4^sca-537.4, eg^UAS.cDa

hkb², srp³ has embryonic Malpighian tubule phenotype

hkb², srp³ has embryonic/larval midgut primordium phenotype

Scer\GAL4^sca-537.4, eg^UAS.cDa, hkb² has serotonergic neuron phenotype