pnrVX6/pnrMD237 transheterozygous adults displaying thoracic clefts and loss of dorsocentral mechanosensory macrochaetae, as compared to wild-type controls.
Class I abdominal dorsal multidendritic ddaD and ddaE neurons from pnrVX6 mutant somatic clones in third instar larvae present misoriented dendrite branch terminals, as compared to controls.
pnrVX6/+ ; Df(3R)Exel6157/+ double heterozygous embryos show asymmetric cell division defects in "svp" cardiac progenitor cells that are not significantly different from the additive effects of each of the two single heterozygotes. Defects in the symmetric cell divisions that give rise to the tin-expressing cardial cells in the double heterozygotes are not significantly different from the additive effects of each of the two single heterozygotes.
pnrVX6/+ ; Df(1)CHES-1-like1/+ double heterozygous embryos show asymmetric cell division defects in "svp" cardiac progenitor cells that are not significantly different from the additive effects of each of the two single heterozygotes. Defects in the symmetric cell divisions that give rise to the tin-expressing cardial cells in the double heterozygotes are not significantly different from the additive effects of each of the two single heterozygotes.
Heterozygotes have a normal number of scutellar bristles.
Herozygotes exhibit a significant decrease in lifespan, as compared to controls.
pnrVX6/+ flies have the normal number of dorsocentral bristles.
Less than 1% of pnrVX6/+ flies show any dorsocentral bristle loss.
In pnrVX6 mutant embryos, only remnants of the heart and lymph gland appear to be present.
pnrVX6 mutant embryos have reduced levels of both myocardial and pericardial cells.
Eye development occurs normally in heterozygous flies. Homozygous clones in the eye disc and adult eye show dorsal eye enlargements.
In stage-15 pnrVX6 mutant embryos, the lymph gland, cardioblasts and pericardial nephrocytes fail to develop from the cardiogenic mesoderm.
In mutant embryos cardioblasts almost never develop, a strong decrease in pericardial cells is also seen.
During mid-stage 11 mutant embryos exhibit a loss of cardiac precursors, cardiogenesis appear not to be initiated. By stage 16 a loss of pericardial cells are seen.
Homozygous clones in the eye result in dorsal eye enlargements or ectopic eye, due to a change of dorsal eye fate to ventral. Eye discs homozygous for pnrVX6 (generated using the "EGUF" method to remove all eye disc cells except the homozygous pnrVX6 clone cells) show dorsal overgrowths in the disc and in adult eyes.
The amnioserosa cells appear morphologically normal until the end of embryogenesis in mutant animals. Germband retraction is normal. Homozygous larvae have a characteristic basket shape and dorsal closure defects. The abdominal region of the cuticle lacks the most dorsal pattern elements (the dorsal triangles), which appear to be replaced by dorsolateral spinules.
Homozygous somatic clones in the lateral (LAT) notal region proliferate and differentiate normally, very few clones are seen in the medial (MED) notal region the few that are seen, are in the process of invaginating from the surrounding tissue. Those clones that extended to both regions differentiate normally in the LAT region but form necrotic tissue in the MED region. In some cases invaginated tissue can be seen to differentiate notum structures. In addition some clones found associated with the LAT region, usually near the MED/LAT border, form invaginating vesicles or outgrowths. In these cases the normal LAT pattern is not altered. Very few clones are seen in the medial abdomen region, as compared to the lateral abdomen. Those clones that are in the medial region are always abnormal. dpo not integrate with wild-type cells and form vesicles that segregate from the surrounding tissue. Nevertheless, they differentiate bristles and cuticle of abdominal character.
Homozygous clones in the eye disc only produce a phenotype when they are at the dorsal margin of the eye disc. These clones result in an ectopic field of differentiating photoreceptors anterior to the main eye field. In adult flies this results in the formation of an ectopic eye field in the dorsal head cuticle, which can either be separate from or fused with the normal eye. These ectopic eye fields do not arise exclusively from mutant cells within the clone itself, but also contain wild-type cells. Duplication of the antenna is also frequently observed. In some cases a dramatic loss of the eye and an absence of differentiating photoreceptors in the eye disc is seen, resulting from the loss of all pnr function, in animals carrying very large homozygous clones in the eye. Most animals carrying large clones in the eye die as late pupae, and their heads are sometimes entirely missing. Homozygous dorsal and ventral clones in the eye which lie close to the equator do not show any polarity defects. Only the largest and most dorsal clones, up to eight ommatidial rows from the equator, are abnormal. Ommatidial clusters in the equatorial regions of these clones adopt a ventral polarity and chirality, and more dorsally, the formation of an ectopic equator is seen. This new equator forms within the clone rather than at its boundary and the polarity inversion does not strictly follow the borders of the clone. On one hand, some mutant clusters near the margins of the clone show normal dorsal polarity, and on the other, wild-type ommatidia adjacent to a mutant clone sometimes show chirality changes.
In female D.simulans/D.melanogaster hybrids heterozygous for pnrVX6 the posterior scutellar bristle, anterior dorsocentral bristle, posterior postalar bristle and the posterior dorsocentral bristle are lost at a high frequency compared to female D.simulans/D.melanogaster hybrid controls, when grown at both 18oC and 25oC (though the effect is stronger at 25oC. In female D.simulans/D.melanogaster hybrids heterozygous for pnrVX6 and Df(1)sc-B57, the posterior and anterior scutellar bristles and the posterior and anterior dorsocentral bristles are lost at a high frequency compared to female D.simulans/D.melanogaster hybrid with pnrVX6 or Df(1)sc-B57 alone.
In(3R)iab6G/pnrVX6 flies are lethal as pupae and have strong imaginal defects. Mitotic clones in the thorax adjacent to the thoracic midline cause a sizeable bilateral cleft involving most of the scutum causing the entire scutellum to disappear.
Cells of the amnioserosa and part of the dorsal epidermis die. The phenotype in clones is similar to that of pnrD1.