Temperature adaptation of soil bacterial communities along an Antarctic climate gradient: predicting responses to climate warming

Soil microorganisms, the central drivers of terrestrial Antarctic ecosystems, are being confronted with increasing temperatures as parts of the continent experience considerable warming. Here we determined short‐term temperature dependencies of Antarctic soil bacterial community growth rates, using the leucine incorporation technique, in order to predict future changes in temperature sensitivity of resident soil bacterial communities. Soil samples were collected along a climate gradient consisting of locations on the Antarctic Peninsula (Anchorage Island, 67 °34′S, 68 °08′W), Signy Island (60 °43′S, 45 °38′W) and the Falkland Islands (51 °76′S 59 °03′W). At each location, experimental plots were subjected to warming by open top chambers (OTCs) and paired with control plots on vegetated and fell‐field habitats. The bacterial communities were adapted to the mean annual temperature of their environment, as shown by a significant correlation between the mean annual soil temperature and the minimum temperature for bacterial growth (T_min). Every 1 °C rise in soil temperature was estimated to increase T_min by 0.24–0.38 °C. The optimum temperature for bacterial growth varied less and did not have as clear a relationship with soil temperature. Temperature sensitivity, indicated by Q₁₀ values, increased with mean annual soil temperature, suggesting that bacterial communities from colder regions were less temperature sensitive than those from the warmer regions. The OTC warming (generally <1 °C temperature increases) over 3 years had no effects on temperature relationship of the soil bacterial community. We estimate that the predicted temperature increase of 2.6 °C for the Antarctic Peninsula would increase T_min by 0.6–1 °C and Q₁₀ (0–10 °C) by 0.5 units.     

Distinct gene subsets in pterygia formation and recurrence: dissecting complex biological phenomenon using genome wide expression data

Background

Pterygium is a common ocular surface disease characterized by fibrovascular invasion of the cornea and is sight-threatening due to astigmatism, tear film disturbance, or occlusion of the visual axis. However, the mechanisms for formation and post-surgical recurrence of pterygium are not understood, and a valid animal model does not exist. Here, we investigated the possible mechanisms of pterygium pathogenesis and recurrence.

Methods

First we performed a genome wide expression analysis (human Affymetrix Genechip, >22000 genes) with principal component analysis and clustering techniques, and validated expression of key molecules with PCR. The controls for this study were the un-involved conjunctival tissue of the same eye obtained during the surgical resection of the lesions. Interesting molecules were further investigated with immunohistochemistry, Western blots, and comparison with tear proteins from pterygium patients.

Results

Principal component analysis in pterygium indicated a signature of matrix-related structural proteins, including fibronectin-1 (both splice-forms), collagen-1A2, keratin-12 and small proline rich protein-1. Immunofluorescence showed strong expression of keratin-6A in all layers, especially the superficial layers, of pterygium epithelium, but absent in the control, with up-regulation and nuclear accumulation of the cell adhesion molecule CD24 in the pterygium epithelium. Western blot shows increased protein expression of beta-microseminoprotein, a protein up-regulated in human cutaneous squamous cell carcinoma. Gene products of 22 up-regulated genes in pterygium have also been found by us in human tears using nano-electrospray-liquid chromatography/mass spectrometry after pterygium surgery. Recurrent disease was associated with up-regulation of sialophorin, a negative regulator of cell adhesion, and never in mitosis a-5, known to be involved in cell motility.

Conclusion

Aberrant wound healing is therefore a key process in this disease, and strategies in wound remodeling may be appropriate in halting pterygium or its recurrence. For patients demonstrating a profile of 'recurrence', it may be necessary to manage as a poorer prognostic case and perhaps, more adjunctive treatment after resection of the primary lesion.     

The genetic diversity and evolution of field pea (<Emphasis Type="Italic">Pisum</Emphasis>) studied by high throughput retrotransposon based insertion polymorphism (RBIP) marker analysis

Background  

The genetic diversity of crop species is the result of natural selection on the wild progenitor and human intervention by ancient and modern farmers and breeders. The genomes of modern cultivars, old cultivated landraces, ecotypes and wild relatives reflect the effects of these forces and provide insights into germplasm structural diversity, the geographical dimension to species diversity and the process of domestication of wild organisms. This issue is also of great practical importance for crop improvement because wild germplasm represents a rich potential source of useful under-exploited alleles or allele combinations. The aim of the present study was to analyse a major Pisum germplasm collection to gain a broad understanding of the diversity and evolution of Pisum and provide a new rational framework for designing germplasm core collections of the genus.     

GROWTH, MORTALITY AND FECUNDITY IN SUCCESSIVE GENERATIONS OF HEIX ASERSA MULLER CULTURED INDOORS AND CROWDING EFFECTS ON FAST-, MEDIUM- AND SLOW-GROWING SNAILS OF THE SAME CLUTCH

This paper examines the optimum conditions for edible snailsHelix aspersa to be cultured indoors successfully in successivegenerations (originating from the crossing of snails comingfrom different clutches of a previous generation), and the effectof crowding on growth and reproduction in fast-, medium-, andslow-growing snails coming from the same clutches. The timeneeded for the snails to reach marketable size (25–32mm)varied from 2.5 to 5 months up to the 7th generation. The timeneeded for the snails to mature and reproduce from 4 to 7 monthsuntil the fifth generation. After the F5 x F5 generation, thefinal size of the snails decreased. The number of eggs did notdiffer statistically among the different generations but thereproductive success (how many snails reproduced/cage) increasedfrom Fl = Fl generation onwards to F5 x F5. In F6 x F6 onlythree (out of 26) snails reproduced and in F7 x F7 none, althoughthe snails remained under controlled conditions for 15 moremonths. Mortality in the different generations varied from 0–10%up to F5 x F5 but from F6 x F6 onwards increased and reached25%. Concerning the origin of snails, it was found that largersnails (originating from Kyparissia, Peloponnesos) lay statisticallymore eggs (138.40 ± 29.60, N =5) than smaller ones (77.38± 40.42, N=4) (originating from Hania, island of Crete).Hatching success was greater, too. (Received 10 September 1996; accepted 24 March 1997)     

Isolation of Aspergillus nidulans Mutants That Overcome brlA-Induced Growth Arrest

The Aspergillus nidulans brlA gene is a primary regulator of development-specific gene expression during conidiation. Forced activation of brlA in vegetative cells leads to inappropriate induction of conidiophore formation and causes growth to stop. In fact, when conidia containing a nutritionally inducible brlA gene fusion are placed on inducing medium, they fail to germinate. We used this phenotype to select 174 mutants that continue growing following such forced brlA activation. Forty-six of these mutants also produced abnormal developmental structures during air-induced conidiation as expected if the mutations resulted in an altered response to BrlA (designated sbr mutants for suppressors of brlA response). The predominant mutant class identified was defective in a known developmental regulatory gene, abaA. We also identified mutants with defects in the previously characterized early acting developmental regulatory genes flbB and flbD and in four previously undescribed loci designated sbrA-D. sbrA mutants represent the second largest group and are characterized by production of conidiophore stalks that lack a normal vesicle and form branching sterigmata that rarely make spores. Because abaA expression could not be detected in sbrA mutants following brlA activation we propose that sbrA functions as a developmental modifier, participating in brlA-dependent activation of other developmental regulators.     

La dormance embryonnaire chez Taxus baccata: Influence de la composition du milieu liquide sur I'induction de la germination Par

Embryo dormancy of Taxus baccata var. fastigiata is eliminated when cultured continuously in nutritive liquid medium. An equivalent percentage of germination is obtained when the embryos are transferred to agar medium after 8 days of liquid culture. There is no morphological development of the embryo during the period in the liquid medium. But we have ascertained that water-soluble germination inhibitors present in the embryo are leached out into the medium, permitting germination. Germination is totally absent when the embryos are cultured continuously in distilled water, alone or with minerals; incidental in sucrose solution; and maximal when the medium contains sucrose and Ca²⁺ or K⁺ ions. The extent of germination on agar medium depends upon the composition of the liquid medium in which the embryos are cultured for the initial 8 days. But this preliminary culture in the liquid medium does not always remove the endogenous inhibitors, irrespective of its composition. This can be achieved only in the presence of sucrose; and this process can be made more effective by the addition of Ca²⁺ ions.     

Facilitated Penetration of Amanitin—Albumin Conjugates into Hepatocytes after Coupling with Fluorescein

α-AMANITIN, a cyclic peptide of the toadstool Amanita phalloides^1,2, causes necrosis of liver and kidney cells, the first morphological lesions occurring in the nuclei^3,4. It acts by binding to RNA polymerase in eukaryotic .cells and inhibiting the enzyme^5–9. The hepatotoxicity of amanitin increases several times when it is conjugated to albumin, probably because of a slower rate of elimination of the toxin through the glomeruli^4,10. It is unlikely that the amanitin-albumin conjugate enters the hepatocyte by a mechanism involving its albumin moiety; it was therefore suggested¹¹ that penetration of the liver cells is consequent on binding of the amanitin group to the carrier involved in transport of this peptide. This led us to consider more generally the facilitation of penetration into cells by large molecules by means of binding to another molecule for which a carrier exists on the cell membrane^12,13.     

Rapid site-specific DNA inversion in Escherichia coli mutants lacking the histonelike protein H-NS.

Escherichia coli pilG mutants are thought to have a dramatically higher DNA inversion rate as measured by the site-specific DNA inversion of the type 1 pili pilA promoter. DNA sequence of the pilG gene confirmed its identity to the gene encoding the bacterial histonelike protein H-NS. Unlike other histonelike protein complexes that enhance site-specific DNA recombination, the H-NS protein inhibited this process. This inhibition was indicated by the increased inversion rate of the pilA promoter region effected by two different mutant pilG alleles. One of these alleles, pilG1, conferred a mutant phenotype only at low temperature attributable to a T-to-G transversion in the -35 sequence of the pilG promoter. The other allele, pilG2-tetR, was an insertion mutation in the pilG coding region that conferred the mutant phenotype independent of temperature. We measured an approximately 100-fold-increased pilA promoter inversion rate in the mutant by exploiting the temperature-dependent expression of pilG1 and using a novel rapid-population-sampling method. Contrary to one current view on how the H-NS protein might act to increase DNA inversion rate, we found no evidence to support the hypothesis that DNA supercoiling affected pilA promoter inversion.