drprΔ5 homozygous mutant stage 14 egg chambers show nurse cell clearance defect and contain persistent nurse cell nuclei, while in wild-type egg chambers all the germ-line derived nurse cells have undergone programmed cell death and been cleared by this stage.
drprΔ5 mutants do not display any significantly reduced survival when infected with Leishmania amastigotes, as compared to wild type.
Homozygous adults are short lived and show an age-dependent decline in locomotor activity in a negative geotaxis assay, as compared to age-matched controls.
30 day old homozygous adults sometimes show defects in the jump muscle of the thorax, including hyalinization with loss of striation, vacuolisation and variable muscle fiber size. The flight muscles appear normal. Degeneration is also seen in the brain and retina.
drprΔ5/Df(3L)BSC181 mutant pupae exhibit defects in phagocytic clearance of ddaC neuron dendrite debris following pupal stage dendritic pruning. Similarly, unlike in wild type, drprΔ5/Df(3L)BSC181 mutant larvae in which the dendrites have been injured (severed with an infrared laser) exhibit defects in debris clearance.
Homozygous drprΔ5 mutant flies are unable to clear axonal debris from L1 wing vein neurons following axotomy.
In the posterior abdominal region of the ventral nerve cord at 6 hours after pupal formation, drprΔ5 mutants exhibit similar numbers of astrocytic vacuoles compared with controls, although vacuole size is significantly reduced (by ~50% compared to controls).
drprΔ5 mutants exhibit a significant amount of brp[+] debris in the abdominal region of the ventral nerve cord.
drprΔ5 mutants exhibit a strong suppression of mushroom body γ neuron pruning at 18 hours after pupal formation and a mild phenotype in adults.
Under normal nutritional conditions drprΔ5 mutant egg chambers develop normally through mid-oogenesis. However, when degenerating egg chambers are induced by starvation drprΔ5 mutant flies show significant defects in the normal engulfment of dying germline cells. Unlike in wild type, the follicle cells fail to enlarge as nurse cell chromatin condenses, and minimal uptake of nuclear fragments is seen. As egg chamber death progresses, the follicle cells die without clearing most of the nurse cell debris.
The majority of drprΔ5 mutant germline clones in starvation-induced degenerating egg chambers are able to undergo proper follicle cell engulfment of germline debris, although some do show some aberrant engulfment.
Dispersed hemocytes derived from drprΔ5 embryos show a significantly reduced level of phagocytosis of apoptotic cells compared to wild type.
Axonal debris from severed ORN axons is not cleared in drprΔ5 mutants, indicating a defect in glial engulfment.
The pruning of gamma neurons of larval mushroom bodies during metamorphosis is severely impaired in drprΔ5 mutants.
drprΔ5 mutant embryonic hemocytes show decreased competence to undertake phagocytosis of apoptotic cells, as compared to controls. These mutants do not show a delay in development to adulthood, as compared to controls.
98% of drprΔ5 homozygous pupae display persistent salivary gland material.
Larval hemocytes prepared from drprΔ5 flies less effectively phagocytose the parental S. aureus strain, compared with hemocytes of wild type flies. In contrast to wild type, phagocytosis of the mutant 'ItaS' S. aureus strain by drprΔ5 hemocytes is equal to that of the parental strain. In vivo assays of drprΔ5 flies produce the same results.
A S. aureus strain lacking WTA is less effectively phagocytosed than the parental S. aureus strain by hemocytes prepared from drprΔ5 flies.
B. subtilis and E. coli are less effectively phagocytosed by hemocytes prepared from drprΔ5 flies compared to wild type hemocytes.
drprΔ5 flies infected with the parental S. aureus strain die earlier than control flies. drprΔ5 flies show increased growth of the bacteria compared to controls.
The level of phagocytosis occurring in hemocytes of mutant embryos is reduced compared to controls.
The number and total volume of apoptotic particles in the central nervous system (CNS) is increased about 2-fold compared to wild type. There is no significant defect in engulfment, with the fraction of untouched particles being similar to that seen in the wild type. Instead, the excess particles accumulate in the phagocytes.
Mutants show defects in glial phagocytic function; significant amounts of axonal debris remain within Or85e-innervated glomeruli and in the maxillary nerve 5 days after ablation of maxillary palps in heterozygous and homozygous animals, in contrast to control animals.
Homozygous stage 14-15 embryos show a marked increase in the number of central nervous system cell corpses (38.5 cell corpses per hemisegment) compared to control embryos (24.4 cell corpses per hemisegment).
Homozygous clones grow equivalently to wild-type twin spots.
Pruning of the larval axon branches of the γ neurons is suppressed in mutants, such that many of the larval axons persist in mutant pupae at 18 hours after puparium formation (APF). The larval γ neuron branches persist in both the dorsal and medial lobes at 24 and 48 hours after puparium formation, though their total volume appears to decrease. Abnormal axon branches are seen outside of the α/β lobes in 1 week old mature adults, which appear (from analysis of marker expression) to be the remnants of the larval γ neurons. In addition, fusion of the β lobes is seen after 48 hours APF in the mutant animals.
At 6 and 18 hours APF, the volume of the distal tip region of the mushroom body dorsal lobes which is infiltrated by glial processes is decreased in mutants compared to wild type. The number of glial lumps over 2 μM per mushroom body lobe is severely reduced in the mutants compared to wild type at these timepoints (these lumps are normally formed by glial processes that engulf clusters of varicosities on the axon branches), and glial lumps are observed only near the periphery of the mutant mushroom body lobes in the vicinity of the glial cell bodies.
Antennal lobe glia show no noticeable changes in morphology when the third antennal segment is ablated in drprΔ5 mutants. Antennal lobe morphology is grossly normal in drprΔ5 mutants.
In wild-type controls, ablation of the maxillary palps leads to enrichment of glial membranes with maxillary palp-innervated glomeruli. However, this is blocked in drprΔ5 mutants. Glial processes do not accumulate in glomeruli housing severed maxillary palp ORN axons nor are they recruited at high levels to the maxillary nerve.
The majority of axonal debris lingered in the CNS of drprΔ5 mutants after ablation of the third antennal segments. Three days after injury there is an abundance of axon fibers remaining in the antennal lobes. Five days after injury in drprΔ5 mutants, approximately 65% of antennal lobes retain axonal fibers. Severed axon fragmentation is not blocked in drprΔ5 mutants. Severed axons show signs of fragmentation as early as 5 hours after injury in drprΔ5 mutants.
In flies homozygous for drprΔ5, dendrite branch removal is strongly suppressed despite clear evidence of severing.