Third instar larvae expressing htlDN.UAS.cMb under the control of Scer\GAL4repo.PU exhibit fewer glial nuclei along peripheral nerves, where no bulges are observed, as compared to controls.
Expression of htlDN.Scer\UAS.cMb in retinal basal glial (RBG) cell clones under the control of Scer\GAL4repo results in a reduction in RBG cell number, loss of differentiation and lack of migration in third instar larvae.
Expression of htlDN.Scer\UAS.cMb in the longitudinal visceral muscle (LVM) founder cells under the control of Scer\GAL4tey-5053A results in a reduction in the number of founder cells and cell death close to the trunk visceral mesoderm (TVM). LVM founder cell migration is incomplete.
Expression of htlDN.Scer\UAS.cMb driven by Scer\GAL4how-24B significantly reduces the number of boutons per muscle at the neuromuscular junction of third instar larvae, compared to controls.
Evoked excitatory junction potential (EJP) and miniature EJP (mEJP) amplitude are significantly increased (there is no significant difference in quantal content or mEJP frequency) at the NMJ of Scer\GAL4how-24B>htlDN.Scer\UAS.cMb third instar larvae, compared to controls.
Expression of htlDN.Scer\UAS.cMb under the control of Scer\GAL4repo results in a reduction in glial cell number and impaired glial migration in the eye disc.
Expression of htlDN.Scer\UAS.cMb under the control of Scer\GAL41151 results in a decrease in the number of founder cells per hemisegment compared to wild-type hemisegments; in 49% of Scer\GAL41151>htlDN.Scer\UAS.cMb hemisegments there are ~4 founder cells instead of the wild-type range of 17-22 and in 17% of hemisegments dorsal founders are completely absent. The number of myoblasts is not affected.
Individuals expressing htlDN.Scer\UAS.cMb exhibit abnormal pathfinding behaviour in ocellar pioneer (OP) and bristle mechanosensory (BM) axons in a dose dependant manner. This phenotype is enhanced by the addition of htlAB42. The axon guidance and extension alterations seen in htlDN.Scer\UAS.cMb individuals can be sorted into five different types. In type a, before head eversion OP axons spread abnormally, after head eversion OP axons can be seen to follow the trajectory of the BM axons. The type b defect consists of OP axons that extend normally detached from the epithelium but are unable to cross to the brain at the normal choice point. Instead they continue extending along the head contour. This type of defect is sometimes seen when one copy of htlDN.Scer\UAS.cMb is driven by Scer\GAL4sca-537.4, it is seen in all cases when 2 copies are driven. After head eversion this alteration results in an OP nerve that projects away from the epoidermal surface inside the head and reaches an ectopic position (sometimes terminating in the fat tissue in front of the brain.) The type c phenotypic class includes the BM axons. These axons always initially extend in the correct orientation, but when reaching the appropriate choice point just dorsal to the antena, they fail to detach from the epidermis and fail to cross and project into the brain. INstead they turn on themselves or on other converging BM axons and project backwards. Remarkably, these BM axons can sometimes perforate the epithelium and project outside the head, in the space between the old pupal cuticle molt and the newly deposited adult cuticle. Less frequently BM axons can be observed stalling in the epidermis or extending abnormally separated from the epidermal surface.
Embryos expressing htlDN.Scer\UAS.cMb under the control of both Scer\GAL4twi.PG and Scer\GAL4Mef2.PR show partial loss of cardial cells, pericardial cells and somatic muscles. Small gaps in the normally continuous rows of visceral mesoderm progenitors are also seen. These embryos show normal early mesoderm dorsolateral migration.