Glycolysis regulates Hedgehog signalling via the plasma membrane potential.

Changes in cell metabolism and plasma membrane potential have been linked to shifts between tissue growth and differentiation, and to developmental patterning. How such changes mediate these effects is poorly understood. Here, we use the developing wing of Drosophila to investigate the interplay between cell metabolism and a key developmental regulator-the Hedgehog (Hh) signalling pathway. We show that reducing glycolysis both lowers steady-state levels of ATP and stabilizes Smoothened (Smo), the 7-pass transmembrane protein that transduces the Hh signal. As a result, the transcription factor Cubitus interruptus accumulates in its full-length, transcription activating form. We show that glycolysis is required to maintain the plasma membrane potential and that plasma membrane depolarization blocks cellular uptake of N-acylethanolamides-lipoprotein-borne Hh pathway inhibitors required for Smo destabilization. Similarly, pharmacological inhibition of glycolysis in mammalian cells induces ciliary translocation of Smo-a key step in pathway activation-in the absence of Hh. Thus, changes in cell metabolism alter Hh signalling through their effects on plasma membrane potential.

Drosophila jumu modulates apoptosis via a JNK-dependent pathway and is required for other processes in wing development.

Previous studies in several model organisms have revealed that members of the Forkhead (Fkh) transcription factor family have multiple functions. Drosophila Jumeau (Jumu), a member of this family, participates in cardiogenesis, hematopoiesis and immune system homeostasis. Here, we show that loss of jumu function positively regulates or triggers apoptosis via a JNK-dependent pathway in wing development. jumu mutants showed reduced wing size and increased apoptosis. Moreover, we observed a loss of the anterior cross vein (ACV) phenotype that was similar to that observed in wings in which JNK signaling has been ectopically activated. The JNK signaling markers puckered (puc) and p-JNK were also significantly increased in the wing discs of jumu mutants. In addition, apoptosis induced by the loss of jumu was rescued by knocking down JNK, indicating a role for JNK in reducing jumu-induced apoptosis. Jumu could also control wing margin development via the positive regulation of cut expression, and the observed wing margin defect did not result from a loss of jumu-induced apoptosis. Further, jumu deficiency in the pupal wing could induce multiple wing hairs via a Rho1-mediated planar cell polarity pathway, but abnormal Rho1 expression was not why jumu loss induced apoptosis via a JNK-dependent pathway in wing discs.

Deformed Wing Virus Infection in Honey Bees (Apis mellifera L.).

Deformed wing virus (DWV) is a single-stranded RNA virus of honey bees (Apis mellifera L.) transmitted by the parasitic mite Varroa destructor. Although DWV represents a major threat to honey bee health worldwide, the pathological basis of DWV infection is not well documented. The objective of this study was to investigate clinicopathological and histological aspects of natural DWV infection in honey bee workers. Emergence of worker honey bees was observed in 5 colonies that were clinically affected with DWV and the newly emerged bees were collected for histopathology. DWV-affected bees were 2 times slower to emerge and had 30% higher mortality compared to clinically normal bees. Hypopharyngeal glands in bees with DWV were hypoplastic, with fewer intracytoplasmic secretory vesicles; cells affected by apoptosis were observed more frequently. Mandibular glands were hypoplastic and were lined by cuboidal epithelium in severely affected bees compared to tall columnar epithelium in nonaffected bees. The DWV load was on average 1.7 × 106 times higher (P < .001) in the severely affected workers compared to aged-matched sister honey bee workers that were not affected by deformed wing disease based on gross examination. Thus, DWV infection is associated with prolonged emergence, increased mortality during emergence, and hypoplasia of hypopharyngeal and mandibular glands in newly emerged worker honey bees in addition to previously reported deformed wing abnormalities.

Impact of Varroa destructor and deformed wing virus on emergence, cellular immunity, wing integrity and survivorship of Africanized honey bees in Mexico.

The ectoparasitic mite Varroa destructor is the primary health problem of honey bees (Apis mellifera) worldwide. Africanized honey bees in Brazil have demonstrated tolerance to the mite, but there is controversy about the degree of mite tolerance of Africanized bees in other countries. This study was conducted to quantify the effect of V. destructor parasitism on emergence, hemocyte concentration, wing integrity and longevity of Africanized honey bees in Mexico. Africanized bee brood were artificially infested with V. destructor mites and held in an incubator until emergence as adults and compared to non-infested controls. Deformed wing virus (DWV) presence was determined in the mites used to infest the bees. After emergence, the bees were maintained in an incubator to determine survivorship. The percentage of worker bees that emerged from parasitized cells (69%) was significantly lower than that of bees emerged from non-infested cells (96%). Newly-emerged parasitized bees had a significantly lower concentration of hemocytes in the hemolymph than non-parasitized bees. Additionally, the proportion of bees with deformed wings that emerged from V. destructor-parasitized cells was significantly higher (54%) than that of the control group (0%). The mean survival time of bees that emerged from infested and non-infested cells was 8.5 ±â€¯0.3 and 14.4 ±â€¯0.4 days, respectively, and the difference was significant. We conclude that V. destructor parasitism and DWV infections kill, cause deformities and inhibit cellular immunity in developing Africanized honey bees, and significantly reduce the lifespan of adult bees in Mexico. These results suggest that the tolerance of Africanized bees to V. destructor is related to adult bee mechanisms.

Successful Management of Open, Contaminated Metacarpal Fractures in an Adult Snowy Owl ( Bubo scandiacus) With a Minimal Type II External Skeletal Fixator.

An adult, male snowy owl ( Bubo scandiacus) was found down and unable to fly in western New York State. Physical examination and radiographs revealed a subacute, open wound and fractured major and minor metacarpals of the right wing. A minimal type II external skeletal fixator (ESF) device was placed on the right major metacarpal bone and the open wound was allowed to granulate and close. After evidence of bone union, the ESF device was removed. The owl performed auto-physiotherapy throughout the process and was released with sustained flight 2 months postoperatively. It was recaptured 7 weeks later and underwent further rehabilitation to allow successful release 11 months after surgical stabilization. To our knowledge, this is the first case report describing use of a type II ESF device on the metacarpus of a bird.

Use of a Compounded Poloxamer 407 Antibiotic Topical Therapy as Part of the Successful Management of Chronic Ulcerative Dermatitis in a Congo African Grey Parrot ( Psittacus erithacus).

A 23-year-old, 425-g male African grey parrot ( Psittacus erithacus) was evaluated for chronic ulcerative dermatitis of the axillary regions under both wings. Initial swab cultures of the sites had revealed a coagulase-positive methicillin-resistant Staphylococcus aureas (MRSA) with marked antibiotic resistance. A second swab culture obtained 8 weeks after the initial culture showed heavy growth of a coagulase-positive Staphylococcus species, which could not be speciated, but showed the same sensitivity as the previous culture. Previous treatment included systemic antibiotics and a topical antimicrobial cream, with variable response and only temporary resolution. On examination, full-thickness, ulcerative, necrotic dermatitis was present under both wings with intermittent bleeding and subdermal tissue exposure. Initial treatment included wound debridement, oral antibiotics, topical therapy, analgesics, and bandages. After a relapse, a poloxamer gel containing 2% doxycycline, 1% chloramphenicol, and 0.5% mupirocin was used in combination with oral antibiotics and analgesics. On follow-up examination, the skin lesions had completely resolved and the patient was doing well and remains normal 4 years later. This report emphasizes the importance of prompt, aggressive multi-modal therapy for MRSA and other dermal bacterial infections in pet birds that may represent zoonoses or have carrier-state zoonotic potential. Preparation by a compounding pharmacy of a transdermal poloxamer gel containing antibiotics shows promise for severe, infected, ulcerative skin lesions in birds when other therapies fail to achieve a cure.

Experimental infection of bats with Geomyces destructans causes white-nose syndrome.

White-nose syndrome (WNS) has caused recent catastrophic declines among multiple species of bats in eastern North America. The disease's name derives from a visually apparent white growth of the newly discovered fungus Geomyces destructans on the skin (including the muzzle) of hibernating bats. Colonization of skin by this fungus is associated with characteristic cutaneous lesions that are the only consistent pathological finding related to WNS. However, the role of G. destructans in WNS remains controversial because evidence to implicate the fungus as the primary cause of this disease is lacking. The debate is fuelled, in part, by the assumption that fungal infections in mammals are most commonly associated with immune system dysfunction. Additionally, the recent discovery that G. destructans commonly colonizes the skin of bats of Europe, where no unusual bat mortality events have been reported, has generated further speculation that the fungus is an opportunistic pathogen and that other unidentified factors are the primary cause of WNS. Here we demonstrate that exposure of healthy little brown bats (Myotis lucifugus) to pure cultures of G. destructans causes WNS. Live G. destructans was subsequently cultured from diseased bats, successfully fulfilling established criteria for the determination of G. destructans as a primary pathogen. We also confirmed that WNS can be transmitted from infected bats to healthy bats through direct contact. Our results provide the first direct evidence that G. destructans is the causal agent of WNS and that the recent emergence of WNS in North America may represent translocation of the fungus to a region with a naive population of animals. Demonstration of causality is an instrumental step in elucidating the pathogenesis and epidemiology of WNS and in guiding management actions to preserve bat populations against the novel threat posed by this devastating infectious disease.

The Ste12-like transcription factor MaSte12 is involved in pathogenicity by regulating the appressorium formation in the entomopathogenic fungus, Metarhizium acridum.

Homeodomain transcription factor Ste12 is a key target activated by the pathogenic mitogen-activated-protein kinase pathway, and the activated Ste12p protein regulates downstream gene expression levels to modulate phenotypes. However, the functions of Ste12-like genes in entomopathogenic fungi remain poorly understood and little is known about the downstream genes regulated by Ste12. In this study, we characterized the functions of a Ste12 orthologue in Metarhizium acridum, MaSte12, and identified its downstream target genes. The deletion mutant (ΔMaSte12) is defective in conidial germination but not in hyphal growth, conidiation, or stress tolerance. Bioassays showed that ΔMaSte12 had a dramatically decreased virulence in topical inoculations, but no significant difference was found in intrahemolymph injections when the penetration process was bypassed. The mature appressorium formation rate of ΔMaSte12 was less than 10% on locust wings, with the majority hyphae forming appressorium-like, curved but no swollen structures. Digital gene expression profiling revealed that some genes involved in cell wall synthesis and remodeling, appressorium development, and insect cuticle penetration were downregulated in ΔMaSte12. Thus, MaSte12 has critical roles in the pathogenicity of the entomopathogenic fungus M. acridum, and our study provides some explanations for the impairment of fungal virulence in ΔMaSte12. In addition, virulence is very important for fungal biocontrol agents to control insect pests effectively. This study demonstrated that MaSte12 is involved in fungal virulence but not conidial yield or fungal stress tolerance in M. acridum. Thus, MaSte12 and its downstream genes may be candidates for enhancing fungal virulence to improve mycoinsecticides.

Theory of epithelial sheet morphology in three dimensions.

Morphogenesis during embryo development requires the coordination of mechanical forces to generate the macroscopic shapes of organs. We propose a minimal theoretical model, based on cell adhesion and actomyosin contractility, which describes the various shapes of epithelial cells and the bending and buckling of epithelial sheets, as well as the relative stability of cellular tubes and spheres. We show that, to understand these processes, a full 3D description of the cells is needed, but that simple scaling laws can still be derived. The morphologies observed in vivo can be understood as stable points of mechanical equations and the transitions between them are either continuous or discontinuous. We then focus on epithelial sheet bending, a ubiquitous morphogenetic process. We calculate the curvature of an epithelium as a function of actin belt tension as well as of cell-cell and and cell-substrate tension. The model allows for a comparison of the relative stabilities of spherical or cylindrical cellular structures (acini or tubes). Finally, we propose a unique type of buckling instability of epithelia, driven by a flattening of individual cell shapes, and discuss experimental tests to verify our predictions.

PINK1-mediated phosphorylation of Parkin boosts Parkin activity in Drosophila.

Two genes linked to early onset Parkinson's disease, PINK1 and Parkin, encode a protein kinase and a ubiquitin-ligase, respectively. Both enzymes have been suggested to support mitochondrial quality control. We have reported that Parkin is phosphorylated at Ser65 within the ubiquitin-like domain by PINK1 in mammalian cultured cells. However, it remains unclear whether Parkin phosphorylation is involved in mitochondrial maintenance and activity of dopaminergic neurons in vivo. Here, we examined the effects of Parkin phosphorylation in Drosophila, in which the phosphorylation residue is conserved at Ser94. Morphological changes of mitochondria caused by the ectopic expression of wild-type Parkin in muscle tissue and brain dopaminergic neurons disappeared in the absence of PINK1. In contrast, phosphomimetic Parkin accelerated mitochondrial fragmentation or aggregation and the degradation of mitochondrial proteins regardless of PINK1 activity, suggesting that the phosphorylation of Parkin boosts its ubiquitin-ligase activity. A non-phosphorylated form of Parkin fully rescued the muscular mitochondrial degeneration due to the loss of PINK1 activity, whereas the introduction of the non-phosphorylated Parkin mutant in Parkin-null flies led to the emergence of abnormally fused mitochondria in the muscle tissue. Manipulating the Parkin phosphorylation status affected spontaneous dopamine release in the nerve terminals of dopaminergic neurons, the survivability of dopaminergic neurons and flight activity. Our data reveal that Parkin phosphorylation regulates not only mitochondrial function but also the neuronal activity of dopaminergic neurons in vivo, suggesting that the appropriate regulation of Parkin phosphorylation is important for muscular and dopaminergic functions.

Assessing genotoxicity of diuron on Drosophila melanogaster by the wing-spot test and the wing imaginal disk comet assay.

The aim of this study was to evaluate the genotoxicity of the herbicide diuron in the wing-spot test and a novel wing imaginal disk comet assay in Drosophila melanogaster. The wing-spot test was performed with standard (ST) and high-bioactivation (HB) crosses after providing chronic 48 h treatment to third instar larvae. A positive dose-response effect was observed in both crosses, but statistically reduced spot frequencies were registered for the HB cross compared with the ST. This latter finding suggests that metabolism differences play an important role in the genotoxic effect of diuron. To verify diuron's ability to produce DNA damage, a wing imaginal disk comet assay was performed after providing 24 h diuron treatment to ST and HB third instar larvae. DNA damage induced by the herbicide had a significantly positive dose-response effect even at very low concentrations in both strains. However, as noted for the wing-spot test, a significant difference between strains was not observed that could be related to the duration of exposure between both assays. A positive correlation between the comet assay and the wing-spot test was found with regard to diuron genotoxicity.

Skin disease in captive bats: results of an online survey of zoos and rehabilitators in Europe, North America and Australasia.

BACKGROUND: Bats may be held captive in zoos and breeding programmes, and for rehabilitation due to illness, abandonment or injury. OBJECTIVES: To describe the frequency and characteristics of skin disease in captive bats. METHODS: Zoos (n = 164) in Europe, North America, Australia and New Zealand, Wildlife Disease Association members and rehabilitators were invited to complete online questionnaires on skin lesions and housing. Associations between lesion type and site, frequency, species, age, suspected cause and season, and their association with housing in zoos were tested using chi-squared and two-sample z-tests. RESULTS: Skin lesions were seen by 38.5% (15 of 39) of responding zoos and more frequently by rehabilitators (66.7%, 18 of 27; P = 0.024). Of the total of 153 lesions of any type reported by zoos and rehabilitators, almost two thirds occurred on the pinnae (49 of 153, 32%) or wing membranes (45 of 153, 29%). Amongst pinnal lesions, crusting (27%), swelling and redness (25%) and necrosis (20%) were most frequent. In zoos, pinnal (P = 0.001) and wing lesions (P = 0.045) were associated with "season", being more common in winter. Pruritus was rare but more often reported from rehabilitation centres (12 of 77 observed lesions) than from zoos (1 of 76) (P = 0.0015). Lesions most often affected adult and geriatric bats in zoos, and juveniles and adults in rehabilitation. Eight respondents reported that skin disease necessitated euthanasia in individual bats. There was no significant association between type of housing and lesions. CONCLUSION: Pinnal and wing lesions were common in captive bats, often with necrosis. Further research into the causes is needed to improve health and welfare of captive bats.

Leiomyosarcoma of the Wing in a Vieilott's Fireback Pheasant (Lophura rufa).

A 15-year-old, female Vieilott's fireback pheasant (Lophura rufa) presented with a 2-day history of a drooping right wing. Examination revealed severe soft tissue swelling in the area extending from the right shoulder to the humeral-radio-ulnar joint with associated bruising and feather loss. Results of a complete blood cell count revealed marked heterophilia and lymphocytosis, and results of serum biochemical analysis showed severe increases in creatine kinase and aspartate aminotransferase activities, hypoproteinemia, and hypoalbuminemia. Radiographs revealed osteolytic lesions of the right humerus with pathologic fractures and circumferential soft tissue swelling. Although surgical wing amputation was successful, the bird died the next day while being treated. The mass was diagnosed histologically and immunohistochemically as a leiomyosarcoma. This is the first neoplasia of any kind reported in this species, to our knowledge, and one of the very few reports of smooth muscle neoplasms affecting the limb of a bird.

Induction of rapid and selective cell necrosis in Drosophila using Bacillus thuringiensis Cry toxin and its silkworm receptor.

BACKGROUND: Genetic ablation of target cells is a powerful tool to study the origins and functions of cells, tissue regeneration, or pathophysiology in a human disease model in vivo. Several methods for selective cell ablation by inducing apoptosis have been established, using exogenous toxins or endogenous proapoptotic genes. However, their application is limited to cells with intact apoptotic machinery. RESULTS: Herein, we established a method for inducing rapid and selective cell necrosis by the pore-forming bacterial toxin Cry1Aa, which is specifically active in cells expressing the Cry1Aa receptor (CryR) derived from the silkworm Bombyx mori. We demonstrated that overexpressing CryR in Drosophila melanogaster tissues induced rapid cell death of CryR-expressing cells only, in the presence of Cry1Aa toxin. Cry/CryR system was effective against both proliferating cells in imaginal discs and polyploid postmitotic cells in the fat body. Live imaging analysis of cell ablation revealed swelling and subsequent osmotic lysis of CryR-positive cells after 30 min of incubation with Cry1Aa toxin. Osmotic cell lysis was still triggered when apoptosis, JNK activation, or autophagy was inhibited, suggesting that Cry1Aa-induced necrotic cell death occurred independently of these cellular signaling pathways. Injection of Cry1Aa into the body cavity resulted in specific ablation of CryR-expressing cells, indicating the usefulness of this method for in vivo cell ablation. CONCLUSIONS: With Cry toxins from Bacillus thuringiensis, we developed a novel method for genetic induction of cell necrosis. Our system provides a "proteinous drill" for killing target cells through physical injury of the cell membrane, which can potentially be used to ablate any cell type in any organisms, even those that are resistant to apoptosis or JNK-dependent programmed cell death.

Evaluation of Two Miniplate Systems and Figure-of-eight Bandages for Stabilization of Experimentally Induced Ulnar and Radial Fractures in Pigeons ( Columba livia ).

Although plate fixation has advantages over other fixation methods for certain indications, it is rarely used in avian surgery, especially in birds that weigh less than 1000 g. Exceptionally small plating systems for these birds are required, which are relatively expensive and difficult to insert. To study avian fracture healing after repair using miniplates, we evaluated 2 steel miniplate systems in 27 pigeons ( Columba livia ) divided into 4 groups. In each pigeon, the left ulna and radius were transected and the ulna was repaired with a bone plate. In groups A and B, a 1.3-mm adaption plate was applied without and with a figure-of-eight bandage; in groups C and D, a 1.0-mm compression plate was applied without and with a bandage, respectively. Healing was evaluated with radiographs after 3, 14, and 28 days; flight tests were conducted after 14, 21, and 28 days; and the wing was macroscopically examined after euthanasia of birds on day 28. Fractures healed without bending or distortion of the plate in all 27 birds, and no significant differences in healing were found between treatment groups. At the end of the study, 23 pigeons (85.2%) showed good or very good flight ability. Results show the 1.3-mm adaption plate and the 1.0-mm compression plate meet the requirements for avian osteosynthesis and can be recommended for fracture repair of the ulna or other long bones in birds weighing less than 500 g. The application of a figure-of-eight bandage might be beneficial in fracture healing.

Synovial Sarcoma Associated With Indwelling Intramedullary Pin in a Peach-Faced Lovebird (Agapornis roseicollis).

Sarcoma developing in association with a metallic orthopedic procedure is an uncommon but well-recognized complication in mammals. We report on a synovial sarcoma that developed at the site of an intramedullary pin after surgery to treat a bone fracture. A 17-year-old female peach-faced lovebird (Agapornis roseicollis) developed a spherical mass on the distal right dorsal wing at a site that was previously fractured and surgically repaired with an indwelling intramedullary pin. The right wing was amputated at the scapulohumeral joint. One year later, the bird died. Postmortem examination revealed metastases in the right lung, left thoracic wall, and proventricular serosa. Histologically, the tumor had a characteristic biphasic pattern. The tumor was immunohistologically and ultrastructurally identified as a synovial sarcoma. This is the first report of a suspected fracture-associated sarcoma in a bird.

FTD/ALS-associated poly(GR) protein impairs the Notch pathway and is recruited by poly(GA) into cytoplasmic inclusions.

C9ORF72 repeat expansion is the most common genetic mutation in frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS). Abnormal dipeptide repeat proteins (DPRs) generated from repeat-associated non-AUG (RAN) translation of repeat-containing RNAs are thought to be pathogenic; however, the mechanisms are unknown. Here we report that (GR)80 and (PR)80 are toxic in neuronal and non-neuronal cells in Drosophila. In contrast to reported shorter poly(GR) forms, (GR)80 is mostly localized throughout the cytosol without detectable accumulation in the nucleolus, accompanied by suppression of Notch signaling and cell loss in the wing. Some Notch target genes are also downregulated in brains and iPSC-derived cortical neurons of C9ORF72 patients. Increased Notch expression largely suppressed (GR)80-induced cell loss in the wing. When co-expressed in Drosophila, HeLa cells, or human neurons, (GA)80 recruited (GR)80 into cytoplasmic inclusions, partially decreasing the toxicity of (GR)80 and restoring Notch signaling in Drosophila. Thus, different DPRs have opposing roles in cell loss and we identify the Notch pathway as one of the receptor signaling pathways that might be compromised in C9ORF72 FTD/ALS.

Caspase signalling in the absence of apoptosis drives Jnk-dependent invasion.

Tumours evolve several mechanisms to evade apoptosis, yet many resected carcinomas show significantly elevated caspase activity. Moreover, caspase activity is positively correlated with tumour aggression and adverse patient outcome. These observations indicate that caspases might have a functional role in promoting tumour invasion and metastasis. Using a Drosophila model of invasion, we show that precise effector caspase activity drives cell invasion without initiating apoptosis. Affected cells express the matrix metalloprotinase Mmp1 and invade by activating Jnk. Our results link Jnk and effector caspase signalling during the invasive process and suggest that tumours under apoptotic stresses from treatment, immune surveillance or intrinsic signals might be induced further along the metastatic cascade.

The protozoan parasite Trichomonas gallinae causes adult and nestling mortality in a declining population of European Turtle Doves, Streptopelia turtur.

Studies incorporating the ecology of clinical and sub-clinical disease in wild populations of conservation concern are rare. Here we examine sub-clinical infection by Trichomonas gallinae in a declining population of free-living European Turtle Doves and suggest caseous lesions cause mortality in adults and nestlings through subsequent starvation and/or suffocation. We found a 100% infection rate by T. gallinae in adult and nestling Turtle Doves (n = 25) and observed clinical signs in three adults and four nestlings (28%). Adults with clinical signs displayed no differences in any skeletal measures of size but had a mean 3.7% reduction in wing length, with no overlap compared to those without clinical signs. We also identified T. gallinae as the suggested cause of mortality in one Red-legged Partridge although disease presentation was different. A minimum of four strains of T. gallinae, characterized at the ITS/5.8S/ITS2 ribosomal region, were isolated from Turtle Doves. However, all birds with clinical signs (Turtle Doves and the Red-legged Partridge) carried a single strain of T. gallinae, suggesting that parasite spill over between Columbidae and Galliformes is a possibility that should be further investigated. Overall, we highlight the importance of monitoring populations for sub-clinical infection rather than just clinical disease.

Local and systemic effects of targeted zinc redistribution in Drosophila neuronal and gastrointestinal tissues.

While the effects of systemic zinc ion deficiency and toxicity on animal health are well documented, the impacts of localized, tissue-specific disturbances in zinc homeostasis are less well understood. Previously we have identified zinc dyshomeostasis scenarios caused by the targeted manipulation of zinc transport genes in the Drosophila eye. Over expression of the uptake transporter dZIP42C.1 (dZIP1) combined with knockdown of the efflux transporter dZNT63C (dZNT1) causes a zinc toxicity phenotype, as does over expression of dZIP71B or dZNT86D. However, all three genotypes result in different morphologies, responses to dietary zinc, and genetic interactions with the remaining zinc transport genes, indicating that each causes a different redistribution of zinc within affected cells. dZNT86D (eGFP) over expression generates a completely different phenotype, interpreted as a Golgi zinc deficiency. Here we assess the effect of each of these transgenes when targeted to a range of Drosophila tissues. We find that dZIP71B is a particularly potent zinc uptake gene, causing early developmental lethality when targeted to multiple different tissue types. dZNT86D over expression (Golgi-only zinc toxicity) is less deleterious, but causes highly penetrant adult cuticle, sensory bristle and wing expansion defects. The dZIP42C.1 over expression, dZNT63C knockdown combination causes only moderate adult cuticle defects and sensitivity to dietary zinc when expressed in the midgut. The Golgi-only zinc deficiency caused by dZNT86D (eGFP) expression results in mild cuticle defects, highly penetrant wing expansion defects and developmental lethality when targeted to the central nervous system and, uniquely, the fat bodies.