The potential of greenhouse sinks to underwrite improved land management

The current agricultural systems of broad areas of Australia are unsustainable, with large projected increases in salinization, decreases in water quality, wind erosion, and losses of biodiversity. It is well known that these problems can be partially resolved by farmland reforestation; however, a major issue is financing the scale of activity required. The international response to global warming, the United Nations Framework Convention on Climate Change and its Kyoto Protocol, includes provisions that enable greenhouse sinks (sequestration of carbon in soils and vegetation) to be used by parties to fulfil their obligations. The Kyoto Protocol also allows for trading in emission reductions, and this opens the possibility that investment in carbon sinks may help underwrite broader natural resource management objectives. This paper examines the possibilities for improved land management in Western Australia arising from the development of carbon sinks by considering: (a) the likelihood of a carbon market developing and the likely depth of that market as a result of current national and international policies, (b) the data available to provide estimates on different types of sinks, and (c) the likely benefits of wide-scale sink investment.It was estimated that the total amount of carbon that could be sequestered by reforesting 16.8 Mha of cleared farmland is 2200 Mt CO₂-e, and between 290 and 1170 Mt CO₂-e by destocking 94.8 Mha of rangelands. There were insufficient data to produce estimates of sequestration following changes in tillage practice in cropping systems or the revegetation of already salinized land. We conclude that carbon sinks are only likely to become profitable as a broad-scale stand-alone enterprise when carbon prices reach AUD$15/t CO₂-e, with this threshold value varying with carbon yield and project costs. Below this price, their value can be significant as an adjunct to reforestation schemes that are aimed at providing other products (wood, pulp, bioenergy) and land and water conservation benefits. Irrespective of this, carbon sinks provide an opportunity to both sequester carbon in a least-cost fashion and improve soil and watershed management.     

Gene expression, synthesis and degradation of hyaluronan during differentiation of 3T3-L1 adipocytes

The high molecular weight glycosaminoglycan hyaluronan (HA) is an essential component of the extracellular matrix (ECM), however, the link between HA regulation and development of the adipocyte ECM, which is essential for differentiation, remains undefined. Hyaluronan synthase gene expression, HA synthetic rate and molecular weight during differentiation of 3T3-L1 pre-adipocytes were compared to undifferentiated 3T3-L1 pre-adipocytes and non-adipogenic NIH/3T3 fibroblasts. In the 3T3-L1 pre-adipocytes, the predominant genes associated with HA metabolism were found to be HA synthase-2 (Has-2) and hyaluronidase-2 (Hyal-2) demonstrating a co-regulation of expression which was stimulated by adipogenic induction consequently resulting in increased synthesis of high molecular weight HA (>10 MDa) and its simultaneous degradation. Accumulation of HA correlated positively with cell number, although synthetic rate was inversely related suggesting a regulatory feedback mechanism. Within 24h post-induction, pre-adipocytes responded with a higher HA synthetic rate and later, accumulated cytoplasmic lipid. In contrast, undifferentiated pre-adipocytes had a reduced HA synthetic rate during clonal expansion and did not accumulate lipid. HA was continuously and rapidly metabolised throughout 3T3-L1 adipogenesis, where terminal differentiation coincided with the increased generation of low molecular weight, angiogenic HA fragments, a likely prerequisite for concurrent neovascularisation of adipose tissue. This study has highlighted a relationship between HA metabolism and adipocyte differentiation, suggesting that the balance between the formation and regulation of the adipocyte extracellular matrix is finely coordinated in a growth phase-specific dependent manner.     

Murine MusD retrotransposon: structure and molecular evolution of an "intracellularized" retrovirus

We had previously identified active autonomous copies of the MusD long terminal repeat-retrotransposon family, which have retained transpositional activity. These elements are closely related to betaretroviruses but lack an envelope (env) gene. Here we show that these elements encode strictly intracellular virus-like particles that can unambiguously be identified by electron microscopy. We demonstrate intracellular maturation of the particles, with a significant proportion of densely packed cores for wild-type MusD but not for a protease mutant. We show that the molecular origin of this unexpected intracellular localization is solely dependent on the N-terminal part of the Gag protein, which lacks a functional sequence for myristoylation and plasma membrane targeting: replacement of the N-terminal domain of the MusD matrix protein by that of its closest relative-the Mason-Pfizer monkey virus-led to targeting of the MusD Gag to the plasma membrane, with viral particles budding and being released into the cell supernatant. These particles can further be pseudotyped with a heterologous envelope protein and become infectious, thus "reconstituting" a functional retrovirus prone to proviral insertions. Consistent with its retroviral origin, a sequence with a constitutive transport element-like activity can further be identified at the MusD 3' untranslated region. A molecular scenario is proposed that accounts for the transition, during evolution, from an ancestral infectious betaretrovirus to the strictly intracellular MusD retrotransposon, involving not only the loss of the env gene but also an inability to escape the cell--via altered targeting of the Gag protein--resulting de facto in the generation of a very successful "intracellularized" insertional mutagen.     

Right Bundle Branch Block: A Predictor of Mortality in Early Systemic Sclerosis

Objective

To evaluate the prognostic significance of baseline electrocardiogram (ECG) abnormalities in a multiethnic cohort of patients with early systemic sclerosis (SSc) and to determine the serological, clinical, and echocardiogram correlates of ECG findings.

Methods

SSc patients with disease duration of≤5 years were enrolled in the GENISOS (Genetics versus Environment in Scleroderma Outcome Study) cohort. At the first visit, a standard 12 lead ECG was obtained along with demographic information, clinical data, and autoantibodies. The results of echocardiograms were also recorded. All ECGs were interpreted by a cardiologist unaware of the patients'' clinical data.

Results

Of 265 SSc patients with average disease duration at enrollment of 2.5 years, 140 (52.8%) had abnormal ECG findings. These findings were not associated with SSc disease type or autoantibody profile but were associated with more severe heart and lung involvement. A total of 75 patients (28.3%) died over a follow up time of 9.9 years. Complete right bundle branch block (± left anterior hemiblock) on ECG, present in 7 (2.6%) patients, predicted a higher risk of mortality (HR: 5.3; 95% CI: 2.1 to 13.4; p<0.001). The predictive significance of right bundle branch block was independent of age at enrollment, gender, ethnicity and risk factors for coronary artery disease.

Conclusion

ECG abnormalities are common in patients with early SSc and are associated with the severity of lung and heart involvement. Right bundle branch block is an independent predictor of mortality, and should be considered a marker of disease severity in SSc.     

Periplasmic peptidyl prolyl cis-trans isomerases are not essential for viability, but SurA is required for pilus biogenesis in Escherichia coli

In Escherichia coli, FkpA, PpiA, PpiD, and SurA are the four known periplasmic cis-trans prolyl isomerases. These isomerases facilitate proper protein folding by increasing the rate of transition of proline residues between the cis and trans states. Genetic inactivation of all four periplasmic isomerases resulted in a viable strain that exhibited a decreased growth rate and increased susceptibility to certain antibiotics. Levels of the outer membrane proteins LamB and OmpA in the quadruple mutant were indistinguishable from those in the surA single mutant. In addition, expression of P and type 1 pili (adhesive organelles produced by uropathogenic strains of E. coli and assembled by the chaperone/usher pathway) were severely diminished in the absence of the four periplasmic isomerases. Maturation of the usher was significantly impaired in the outer membranes of strains devoid of all four periplasmic isomerases, resulting in a defect in pilus assembly. Moreover, this defect in pilus assembly and usher stability could be attributed to the absence of SurA. The data presented here suggest that the four periplasmic isomerases are not essential for growth under laboratory conditions but may have significant roles in survival in environmental and pathogenic niches, as indicated by the effect on pilus production.     

POFs: what we don't know can hurt us

Over a quarter of all eukaryotic genes encode proteins with obscure features that lack currently defined motifs or domains (POFs). Interestingly, most of the differences in gene repertoire among species were recently found to be attributed to POFs. A comparison of the Arabidopsis, rice and poplar genomes reveals that Arabidopsis contains 5069 POFs, of which 2045 have no obvious homologs in rice or poplar and are likely to be involved in species- or phylogenetic-specific functions in Arabidopsis. The study of POFs is an important endeavor that will shed much needed light on the genetic properties that make any given plant species unique. Furthermore, with respect to many species-specific features, such studies show that we seem to be limited in what we can expect to learn from a model plant such as Arabidopsis.