Differential responses of abandoned wet grassland plant communities to reinstated cutting management

The nature of ecological stability is still debated, and there is a need to establish which types of communities show resistance to environmental change and to explore community responses in relation to their environmental context. This study aims to investigate the effects of reinstating cutting management on abandoned wet grasslands by comparing responses in two different communities with contrasting environmental conditions, to elucidate the restoration potential of wet grasslands. Two coastal wet grassland plant communities in Estonia were monitored over 5?years: a species-poor lower shore grassland and a more diverse tall grassland. Piezometers and soil samples were used to characterise the hydrology, while cutting effects and ongoing abandonment were compared using replicate quadrats in both grasslands. Annual changes and significant differences in community composition were analysed using Detrended and Canonical Correspondence Analyses, diversity indices, and inferential statistics. The results showed that cutting produced greater changes in composition and species abundance in the lower shore community compared to the tall grassland, including a greater proportion of significant differences. The increased responsiveness of the lower shore community may be related to its variable hydrological regime, especially flooding, which creates a dynamic environment favouring adaptable species. In contrast, the tall grassland featured a more stable water regime and species that responded less to perturbation, and manifested resistance to cutting management. Thus, restoring abandoned wet grasslands through vegetation management may be a slow process, especially where there is residual diversity, and the importance of hydrological regime in determining wet grassland communities should be considered.     

Adenosine Stimulates Cone Photoreceptor Myoid Elongation via an Adenosine A2-Like Receptor

In several parts of the nervous system, adenosine has been shown to function as an extracellular neuromodulator binding to surface receptors on target cells. This study examines the possible role of adenosine in mediating light and circadian regulation of retinomotor movements in teleost cone photoreceptors. Teleost cones elongate in the dark and contract in the light. In continuous darkness, the cones continue to elongate and contract at subjective dusk and dawn in response to circadian signals. We report here that exogenous adenosine triggers elongation (the dark/night movement) in isolated cone inner segment-cone outer segment preparations (CIS-COS) in vitro. Agonist/antagonist potency profiles indicate that adenosine's effect on cone movement is mediated by an A2-like adenosine receptor, which like other A2 receptors enhances adenylate cyclase activity. Although closest to that expected for A2 receptors, the antagonist potency profile for CIS-COS does not correspond exactly to any known A2 receptor subtype, suggesting that the cone receptor may be a novel A2 subtype. Our findings are consistent with previous reports that retinal adenosine levels are higher in the dark, and further suggest that adenosine could act as a neuromodulatory "dark signal" influencing photoreceptor metabolism and function in the fish retina.     

Myosin VI is required for structural integrity of the apical surface of sensory hair cells in zebrafish

Unconventional myosins have been associated with hearing loss in humans, mice, and zebrafish. Mutations in myosin VI cause both recessive and dominant forms of nonsyndromic deafness in humans and deafness in Snell's waltzer mice associated with abnormal fusion of hair cell stereocilia. Although myosin VI has been implicated in diverse cellular processes such as vesicle trafficking and epithelial morphogenesis, the role of this protein in the sensory hair cells remains unclear. To investigate the function of myosin VI in zebrafish, we cloned and examined the expression pattern of myosin VI, which is duplicated in the zebrafish genome. One duplicate, myo6a, is expressed in a ubiquitous pattern during early development and at later stages, and is highly expressed in the brain, gut, and kidney. myo6b, on the other hand, is predominantly expressed in the sensory epithelium of the ear and lateral line at all developmental stages examined. Both molecules have different splice variants expressed in these tissues. Using a candidate gene approach, we show that myo6b is satellite, a gene responsible for auditory/vestibular defects in zebrafish larvae. Examination of hair cells in satellite mutants revealed that stereociliary bundles are irregular and disorganized. At the ultrastructural level, we observed that the apical surface of satellite mutant hair cells abnormally protrudes above the epithelium and the membrane near the base of the stereocilia is raised. At later stages, stereocilia fused together. We conclude that zebrafish myo6b is required for maintaining the integrity of the apical surface of hair cells, suggesting a conserved role for myosin VI in regulation of actin-based interactions with the plasma membrane.     

Sulfhydryl oxidases: emerging catalysts of protein disulfide bond formation in eukaryotes

Members of the Quiescin-sulfhydryl oxidase (QSOX) family utilize a thioredoxin domain and a small FAD-binding domain homologous to the yeast ERV1p protein to oxidize sulfhydryl groups to disulfides with the reduction of oxygen to hydrogen peroxide. QSOX enzymes are found in all multicellular organisms for which complete genomes exist and in Trypanosoma brucei, but are not found in yeast. The avian QSOX is the best understood enzymatically: its preferred substrates are peptides and proteins, not monothiols such as glutathione. Mixtures of avian QSOX and protein disulfide isomerase catalyze the rapid insertion of the correct disulfide pairings in reduced RNase. Immunohistochemical studies of human tissues show a marked and highly localized concentration of QSOX in cell types associated with heavy secretory loads. Consistent with this role in the formation of disulfide bonds, QSOX is typically found in the cell in the endoplasmic reticulum and Golgi and outside the cell. In sum, this review suggests that QSOX enzymes play a significant role in oxidative folding of a large variety of proteins in a wide range of multicellular organisms.     

OPTIMIZATION OF THE ENUMERATION OF TOTAL AEROBIC BACTERIAL FLORA IN THE FLESH OF SEAFISH

Abstract The total aerobic flora of seafish flesh is weakly halophilic, and requires on average 1.38% NaCl according to statistical studies. Enumeration is optimal on tryptone soya agar or on NaCl supplemented plate count agar (-H₂S), incubated at 20 and 25C, respectively. Plate count agar (-H₂S) was selected because it can also be used for enumeration of hydrogen sulfide-producing bacteria by degradation of sulfur-containing proteins, which are abundant in fish The models employed are sigmoidal. The initial bioburden is too great for there to be a lag phase during storage in ice at 0C. The models show that when the total aerobic microflora count exceeds 100,000 cfu/g, whole or filleted fish stored on ice at 0C are unfit for consumption.     

OPTIMIZATION OF CULTURE CONDITIONS FOR ENUMERATION OF H2S BACTERIA IN THE FLESH OF SEAFISH

H₂S bacteria of seafish flesh are weakly halophilic and require on average 1.68% NaCl according to statistical studies. Enumeration is optimal on PCA-H₂S(a PCA medium supplemented with sulfur sources and increased NaCl concentrations) incubated at 25C. Total aerobic bacteria can be counted simultaneously on this medium. The proportion of H₂S bacteria relative to total aerobic bacteria increased slightly during prolonged storage of the fish, but was highly variable. Models relating H₂S bacterial counts to spoilage of fish are sigmoidal and showed that when the count exceeds 10,000 CFU/g, whole or filleted fish stored in ice at 0C are unfit for consumption. Shewanella putrefaciens accounted for 69% of the H₂S bacteria at the fifth day of storage and 100% at the fifteenth.     

A single chicken anemia virus protein induces apoptosis.

Chicken anemia virus (CAV) causes cytopathogenic effects in chicken thymocytes and cultured transformed mononuclear cells via apoptosis. Early after infection of chicken mononuclear cells, the CAV-encoded protein VP3 exhibits a finely granular distribution within the nucleus. At a later stage after infection, VP3 forms aggregates. At this point, the cell becomes apoptotic and the cellular DNA is fragmented and condensed. By immunogold electron microscopy VP3 was shown to be associated with apoptotic structures. In vitro, expression of VP3 induced apoptosis in chicken lymphoblastoid T cells and myeloid cells, which are susceptible to CAV infection, but not in chicken embryo fibroblasts, which are not susceptible to CAV. Expression of a C-terminally truncated VP3 induced much less pronounced apoptosis in the chicken lymphoblastoid T cells.     

Enhanced reactivation and enhanced mutagenesis of herpes simplex virus in normal human and xeroderma pigmentosum cells.

Enhanced reactivation (ER) and enhanced mutagenesis (EM) of herpes simplex virus type 1 were studied simultaneously in UV-irradiated stationary cultures of diploid normal human and xeroderma pigmentosum (XP) fibroblasts. Mutagenesis was assayed with unirradiated herpes simplex virus type 1 as a probe in a forward mutation assay (resistance to iododeoxycytidine). Dose-response studies showed that ER increased with the UV dose given to the virus. Optimal reactivation levels were obtained when normal cells and XP variant cells were exposed to a UV dose of 8 J . m-2 and the virus was irradiated with 150 J . m-2. Repair-deficient XP cells of complementation groups A, C, and D showed optimal reactivation levels with a UV dose to the cells of 1.0 J . m-2 and a UV dose to the virus of 40 J . m-2. The time course of appearance of ER and EM was also studied, both in the normal and XP cells. In all cell types except the XP variant cells, EM followed similar kinetics of appearance as did ER. Maximal activities occurred when infection was delayed 1 or 2 days after cell treatment. In XP variant cells, however, maximal expression of the EM function was significantly delayed with respect to ER. The results indicate that ER and EM are transiently expressed in normal and repair-deficient XP cells. Although both phenomena may be triggered by the same cellular event, ER and EM appear to be separate processes that occur independently of each other.     

Effects of cyclic adenosine 3'',5''-monophosphate on photoreceptor disc shedding and retinomotor movement. Inhibition of rod shedding and stimulation of cone elongation

As a test of the hypothesis that cyclic nucleotides play a role in the regulation of retinomotor movements and disc shedding in the photoreceptor-pigment epithelial complex, we have used an in vitro eyecup preparation that sustains both disc shedding and cone retinomotor movements, Eyecups were prepared in white light from animals in which both shedding and cone movement had been blocked by 4 d of constant-light treatment. In eyecups incubated for 3 h in light, disc shedding was negligible and cones remained in the light-adapted (contracted) position. In eyecups incubated in darkness, however, a massive shedding response (dominated by rod photoreceptors) was induced, and at the same time cone photoreceptors elongated to their dark-adapted position. In eyecups incubated in light dbcAMP promoted cone elongation and thus mimicked darkness; the dbcAMP effect was potentiated by the phosphodiesterase inhibitors papaverine and 3- isobutylmethylxanthine. In eyecups incubated in darkness, on the other hand, both phosphodiesterase inhibitors and dbcAMP reduced the phagosome content of the pigment epithelium. The effects of dbcAMP on the cone elongation and rod shedding appear to be specific in that dbcGMP, adenosine, and adenosine 5'-monophosphate had no significant effect. Our results suggest that cAMP plays a role in the regulation of both retinomotor movements and disc shedding.