Impacts of level of utilisation by grazing on an Astrebla (Mitchell grass) grassland in north-western Queensland between 1984 and 2010. 1. Herbage mass and population dynamics of Astrebla spp

Managing large variations in herbage production, resulting from highly variable seasonal rainfall, provides a major challenge for the sustainable management of Astrebla (Mitchell grass) grasslands in Australia. A grazing study with sheep was conducted between 1984 and 2010 on an Astrebla grassland in northern Queensland to describe the effects of a range of levels of utilisation of the herbage at the end of the summer growing season (April–May in northern Australia) on the sustainability of these grasslands. In unreplicated paddocks, sheep numbers were adjusted annually to achieve 0, 10, 20, 30, 50 and 80% utilisation of the herbage mass at the end of the summer over the ensuing 12 months. Higher levels of utilisation reduced both total and Astrebla spp. herbage mass because of the effects of higher utilisation on Astrebla spp. and this effect was accentuated by drought. The tussock density of Astrebla spp. varied widely among years but with few treatment differences until 2005 when density was reduced at the 50% level of utilisation. A major change in density resulted from a large recruitment of Astrebla spp. in 1989 that influenced its density for the remainder of the study. Basal area of the tussocks fluctuated among years, with increases due to rainfall and decreases during droughts. Seasonal rainfall was more influential than level of utilisation in changes to the basal area of perennial grasses. Drought resulted in the death of Astrebla spp. tussocks and this effect was accentuated at higher levels of utilisation. A series of three grazing exclosures were used to examine the recovery of the density and basal area of Astrebla spp. after it had been reduced by 80% utilisation over the preceding 9 years. This recovery study indicated that, although grazing exclusion was useful in the recovery of Astrebla spp., above-average rainfall was the major factor driving increases in the basal area of perennial grasses. Spring values of the Southern Oscillation Index and associated rainfall probabilities were considered to have potential for understanding the dynamics of Astrebla spp. It was concluded that Astrebla grassland remained sustainable after 26 years when grazed at up to 30% utilisation, while, at 50% utilisation, they became unsustainable after 20 years. Results from this study emphasised the need to maintain the population of Astrebla spp. tussocks.

Impacts of level of utilisation by grazing on an Astrebla (Mitchell grass) grassland in north-western Queensland between 1984 and 2010. 2. Plant species richness and abundance

The occurrence of interstitial species in Astrebla grasslands in Australia are influenced by grazing and seasonal rainfall but the interactions of these two influences are complex. This paper describes three studies aimed at determining and explaining the changes in plant species richness and abundance of the interstitial species in a long-term sheep utilisation experiment in an Astrebla grassland in northern Queensland. In the first study, increasing utilisation increased the frequency of Dactyloctenium radulans (Button grass) and Brachyachne convergens (Downs couch) and reduced that of Streptoglossa adscendens (Mint bush). In the second study, seasonal rainfall variation between 1984 and 2009 resulted in large annual differences in the size of the seed banks of many species, but increasing utilisation consistently reduced the seed bank of species such as Astrebla spp. and S. adscendens and increased that of species such as B. convergens, D. radulans, Amaranthus mitchellii (Boggabri) and Boerhavia sp. (Tar vine). In the third study, the highest species richness occurred at the lightest utilisation because of the presence of a range of palatable forbs, especially legumes. Species richness was reduced as utilisation increased. Species richness in the grazing exclosure was low and similar to that at the heaviest utilisation where there was a reduction in the presence of palatable forb species. The pattern of highest species richness at the lightest grazing treatment was maintained across three sampling times, even with different amounts of seasonal rainfall, but there was a large yearly variation in both the density and frequency of many species. It was concluded that the maintenance of highest species richness at the lightest utilisation was not aligned with other data from this grazing experiment which indicated that the maximum sustainable wool production occurred at moderate utilisation.

Disruption of iron homeostasis increases phosphine toxicity in caenorhabditis elegans

The aim of this study is to identify the biochemical mechanism of phosphine toxicity and resistance, using Caenorhabditis elegans as a model organism. To date, the precise mode of phosphine action is unclear. In this report, we demonstrate the following dose-dependent actions of phosphine, in vitro: (1) reduction of ferric iron (Fe3+) to ferrous iron (Fe2+), (2) release of iron from horse ferritin, (3) and the peroxidation of lipid as a result of iron release from ferritin. Using in situ hybridization, we show that the ferritin genes of C. elegans, both ferritin-1 and ferritin-2, are expressed along the digestive tract with greatest expression at the proximal and distal ends. Basal expression of the ferritin-2 gene, as determined by quantitative PCR, is approximately 80 times that of ferritin-1. However, transcript levels of ferritin-1 are induced at least 20-fold in response to phosphine, whereas there is no change in the level of ferritin-2. This resembles the reported pattern of ferritin gene regulation by iron, suggesting that phosphine toxicity may be related to an increase in the level of free iron. Indeed, iron overload increases phosphine toxicity in C. elegans at least threefold. Moreover, we demonstrate that suppression of ferritin-2 gene expression by RNAi, significantly increases sensitivity to phosphine. This study identifies similarities between phosphine toxicity and iron overload and demonstrates that phosphine can trigger iron release from storage proteins, increasing lipid peroxidation, leading to cell injury and/or cell death.