Using Africa's protected area network to estimate the global population of a threatened and declining species: a case study of the Critically Endangered White‐headed Vulture Trigonoceps occipitalis

The White‐headed Vulture Trigonoceps occipitalis (WhV) is uncommon and largely restricted to protected areas across its range in sub‐Saharan Africa. We used the World Database on Protected Areas to identify protected areas (PAs) likely to contain White‐headed Vultures. Vulture occurrence on road transects in Southern, East, and West Africa was adjusted to nests per km² using data from areas with known numbers of nests and corresponding road transect data. Nest density was used to calculate the number of WhV nests within identified PAs and from there extrapolated to estimate the global population. Across a fragmented range, 400 PAs are estimated to contain 1893 WhV nests. Eastern Africa is estimated to contain 721 nests, Central Africa 548 nests, Southern Africa 468 nests, and West Africa 156 nests. Including immature and nonbreeding birds, and accounting for data deficient PAs, the estimated global population is 5475 ‐ 5493 birds. The identified distribution highlights are alarming: over 78% (n = 313) of identified PAs contain fewer than five nests. A further 17% (n = 68) of PAs contain 5 ‐ 20 nests and 4% (n = 14) of identified PAs are estimated to contain >20 nests. Just 1% (n = 5) of PAs are estimated to contain >40 nests; none is located in West Africa. Whilst ranging behavior of WhVs is currently unknown, 35% of PAs large enough to hold >20 nests are isolated by more than 100 km from other PAs. Spatially discrete and unpredictable mortality events such as poisoning pose major threats to small localized vulture populations and will accelerate ongoing local extinctions. Apart from reducing the threat of poisoning events, conservation actions promoting linkages between protected areas should be pursued. Identifying potential areas for assisted re‐establishment via translocation offers the potential to expand the range of this species and alleviate risk.     

Differential synthesis in vitro of barley aleurone and starchy endosperm proteins

To widen the selection of proteins for gene expression studies in barley seeds, experiments were performed to identify proteins whose synthesis is differentially regulated in developing and germinating seed tissues. The in vitro synthesis of nine distinct barley proteins was compared using mRNAs from isolated endosperm and aleurone tissues (developing and mature grain) and from cultured (germinating) aleurone layers treated with abscisic acid (ABA) and GA₃. B and C hordein polypeptides and the salt-soluble proteins β-amylase, protein Z, protein C, the chymotrypsin inhibitors (CI-1 and 2), the α-amylase/subtilisin inhibitor (ASI) and the inhibitor of animal cell-free protein synthesis systems (PSI) were synthesized with mRNA from developing starchy endosperm tissue. Of these proteins, β-amylase, protein Z, and CI- 1 and 2 were also synthesized with mRNA from developing aleurone cells, but ASI, PSI, and protein C were not. CI-1 and also a probable amylase/protease inhibitor (PAPI) were synthesized at high levels with mRNAs from late developing and mature aleurone. These results show that mRNAs encoding PAPI and CI-1 survive seed dessication and are long-lived in aleurone cells. Thus, expression of genes encoding ASI, PSI, protein C, and PAPI is tissue and stage-specific during seed development. Only ASI, CI-1, and PAPI were synthesized in significant amounts with mRNA from cultured aleurone layers. The levels of synthesis of PAPI and CI-1 were independent of hormone treatment. In contrast, synthesis of α-amylase (included as control) and of ASI showed antagonistic hormonal control: while GA promotes and ABA reduces accumulation of mRNA for α-amylase, these hormones have the opposite effect on ASI mRNA levels.     

Bone crushing carnivores and their significance to osteodystrophy in griffon vulture chicks

The natural removal of 89 ungulate carcasses by predators and scavengers was monitored in various wildlife reserves and ranching areas of South Africa. Carnivores responsible for the bone remains were determined. Spotted hyaenas and, to a lesser extent, Brown hyaenas, were the only carnivores that regularly chewed bones. When hyaenas were absent, months of weathering were required before the smaller bones became disarticulated and able to be removed by vultures. The bone-collecting behaviour and related aspects of breeding of two species of griffon vulture were studied at five different nesting colonies in southern Africa—one Cape vulture colony and one White-backed vulture colony in or near wildlife reserves, as well as two Cape vulture colonies and one White-backed vulture colony in ranching land. A total of 2825 bones was found in or below the vulture nests. These bones were categorized and measured. Hyaena-produced bone fragments were found only in the colonies in the wild areas—none of the 387 chicks examined here had osteodystrophy (metabolic bone disease). By contrast, in the ranching areas, vultures collected larger and less fragmented bones. Many Cape vulture chicks had osteodystrophy (130 of 1917 examined), as did two White-backed vulture chicks (of 196 examined). In 1977, artificial feeding stations, 'restaurants' where carcass skeletons were crushed, were established for Cape vultures. Since then, the incidence of osteodystrophy has declined from 17% to 2–5% in 1983. It is clear that bone fragments are an essential dietary requirement, providing calcium for correct skeletal growth of griffon vulture chicks.     

Biosynthesis of penitrems and roquefortine by Penicillium crustosum

Roquefortine and the penitrems were biosynthesised concurrently at an approximately equimolar rate by Penicillium crustosum after growth and sporulation. [14C]mevalonic acid was incorporated (15% efficiency) into the isoprenoid regions of the penitrem and roquefortine molecules to an extent consistent with their 6:1 molar ratio of isoprenoid components. [14C]penitrem A (specific activity, 3.4 X 10(2) mu Ci mmol-1) and 14C-penitrems B, C, and E readministered to young cultures were metabolically interconverted, indicating considerable metabolic flux, though generally directed towards penitrem A as the end product and suggesting a metabolic grid for the penitrem metabolites. Addition of bromide to the medium preferentially favored the production of bromo-analogs rather than the usual chloropenitrems.     

L-Glutamate toxicity in Huntington's disease fibroblasts

Brain degeneration in Huntington's Disease is thought to occur primarily in the regions of high L-glutamate concentrations. Huntington's Disease fibroblast cultures have a sensitivity to these high concentrations of L-glutamate. These cells show degeneration and loss of viability, within 12 hrs, following treatment with 30 mM L-glutamate. This effect appears to be specific for L-glutamate, can be prevented by glutamine, and is not observed in matched control cultures. The observed glutamate sensitivity may serve as a biochemical genetic marker and the excessive effect of glutamate on neuronal membranes could initiate the characteristic neuronal degeneration observed in Huntington's Disease brains.     

Lappet-faced vultures (Torgos tracheliotus) hatch and rear a White-headed vulture (Trigonoceps occipitalis) in the wild

In Gonarezhou National Park, southeast Zimbabwe Rhodesia, White-headed vultures laid their egg in a nest of Lappet-faced vultures in June 1978. Lappet-faced vultures then incubated the egg and reared the nestling successfully to fledging. The chick's feathers however had "fault bars", and during seven days of observation it received less than one visit per day by its foster parents. In the same area in 1973 a White-headed vulture was found incubating its egg in a Lappet-faced vulture style nest. The sizes of these eggs (811 times 650 mm and 79–9 times 65–8 mm) and their estimated dates of laying (24 June 1973 and 21 June 1978) were almost identical, suggesting that the same pair of White-headed vultures was involved.     

Some synthetic phytotoxins structurally related to rhynchosporoside

The (2-O)alpha-d-glucopyranoside of 1,2-propanediol and [U-(14)C]glucose were used as substrates in a reaction with almond beta-glucosidase, which resulted in the production of some (2-O)alpha-d-oligoglucosides of 1,2-propanediol. As its substrate, the beta-glucosidase preferred the glucoside isomer that rotates plane-polarized light to the right. Some of the glucosides produced in the enzymic reaction mixture possessed host selective toxin activity. It appears that the biological activity of the toxin is not dependent on the nature of the glycosidic linkage with the aglycone.     

Tumor necrosis factor and interleukin 1 inhibit parathyroid hormone-responsive adenylate cyclase in clonal osteoblast-like cells by down-regulating parathyroid hormone receptors.

The effects of the monokines tumor necrosis factor alpha (TNF) and interleukin 1 (IL 1) on parathyroid hormone (PTH)-responsive adenylate cyclase were examined in clonal rat osteosarcoma cells (UMR-106) with the osteoblast phenotype. Recombinant TNF and IL 1 incubated with UMR-106 cells for 48 hr each produced concentration-dependent inhibition of PTH-sensitive adenylate cyclase, with maximal inhibition of PTH response (40% for TNF, 24% for IL 1) occurring at 10(-8) M of either monokine. Both monokines also decreased adenylate cyclase stimulation by the tumor-derived PTH-related protein (PTHrP). In contrast, TNF and IL 1 had little or no inhibitory effect on receptor-mediated stimulation of adenylate cyclase by isoproterenol and nonreceptor-mediated enzyme activation by cholera toxin and forskolin; both monokines increased prostaglandin E2 stimulation of adenylate cyclase. Binding of the radioiodinated agonist mono-[125I]-[Nle8,18, Tyr34]bPTH-(1-34)NH2 to UMR-106 cells in the presence of increasing concentrations of unlabeled [Nle8,18, Tyr34]bPTH-(1-34)NH2 revealed a decline in PTH receptor density (Bmax) without change in receptor binding affinity (dissociation constant, Kd) after treatment with TNF or IL 1. Pertussis toxin increased PTH-sensitive adenylate cyclase activity but did not attenuate monokine-induced inhibition of PTH response. In time course studies, brief (1 hr) exposure of cells to TNF or IL 1 during early culture was sufficient to decrease PTH response but only after exposed cells were subsequently allowed to grow for prolonged periods. Inhibition of PTH response by monokines was blocked by cycloheximide. The results indicate that TNF and IL 1 impair responsiveness to PTH (and PTHrP) by a time- and protein synthesis-dependent down-regulation of PTH receptors linked to adenylate cyclase.