Relationships among fire frequency, rainfall and vegetation patterns in the wet–dry tropics of northern Australia: an analysis based on NOAA-AVHRR data

Aim To quantify the regional‐scale spatio‐temporal relationships among rainfall, vegetation and fire frequency in the Australian wet–dry tropics (AWDT). Location Northern Australia: Cape York Peninsula, central Arnhem, central Kimberly, Einasleigh Uplands, Gulf Fall Uplands and northern Kimberley. Methods Monthly ‘fraction of photosynthetic active radiation absorbed by green vegetation’ (fAPAR) was decomposed into monthly evergreen (EG) and monthly raingreen (RG) components using time‐series techniques applied to monthly normalized difference vegetation index (NDVI) data from Advanced Very High Resolution Radiometer (AVHRR) imagery. Fire affected areas were independently mapped at the same spatio‐temporal resolution from AVHRR imagery. Weather station records were spatially interpolated to create monthly rainfall surfaces. Vegetation structural classes were derived from a digitized map of northern Australian vegetation communities (1 : 1,000,000). Generalized linear models were used to quantify relationships among the fAPAR, EG and RG signals, vegetation structure, rainfall and fire frequency, for the period November 1996–December 2001. Results The fAPAR and EG signals are positively correlated with annual rainfall and canopy cover, notably: EG_{closed forest} > EG_{open heathland} > EG_{open forest} > EG_woodland > EG_{open woodland} > EG_{low woodland} > EG_{low open woodland} > EG_{open grassland}. Vegetation height and fAPAR are positively correlated, excluding the special case of open heathland. The RG signal is highest where intermediate annual rainfall and strong seasonality in rainfall coincide, and is associated with vegetation structure as follows: RG_{open grassland} > RG_woodland > RG_{open forest} > RG_{open heathland} > RG_{low woodland} > RG_{open woodland} > RG_{low open woodland} > RG_{closed forest}. Monthly RG tracks monthly rainfall. Annual proportion of area burnt (PB) is maximal where high RG coincides with low EG (open grassland, several woodland communities). PB is minimal in vegetation where both RG and EG are low (low open woodland); and in vegetation where EG is high (closed forest, open heathland). Conclusions The RG–EG scheme successfully reflects digitally mapped tree and grass covers in relation to rainfall. RG–EG patterns are strongly associated with fire frequency patterns. PB is maximal in areas of high RG, where high biomass production during the wet season supports abundant fine fuel during the dry season. PB is minimal in areas with high EG, where relatively moist fuel limits fire ignition; and in areas with low EG and RG, where a relative short supply of fuel limits fire spread.     

A PCR-based molecular marker applicable for marker-assisted selection for anthracnose disease resistance in lupin breeding

Selection for anthracnose disease resistance is one of the major objectives in lupin breeding programs. The aim of this study was to develop a molecular marker linked to a gene conferring anthracnose resistance in narrow-leafed lupin (Lupinus angustifolius L.), which can be widely used for MAS in lupin breeding. A F(8)derived RIL population from a cross between cultivar Tanjil (resistant to anthracnose) and Unicrop (susceptible) was used for marker development. DNA fingerprinting was conducted on 12 representative plants by combining the AFLP method with primers designed based on conserved sequences of plant disease resistance genes. A co-dominant candidate marker was detected from a DNA fingerprint. The candidate marker was cloned, sequenced, and converted into a sequence-specific, simple PCR based marker. Linkage analysis based on a segregating population consisting of 184 RILs suggested that the marker, designated as AntjM2, is located 2.3 cM away from the R gene conferring anthracnose resistance in L. angustifolius. The marker has now being implemented for MAS in the Australian national lupin breeding program.     

Construction of a genetic linkage map using MFLP and identification of molecular markers linked to domestication genes in narrow-leafed lupin (Lupinus angustifolius L.)

A mapping population of F(8)derived recombinant inbred lines (RILs) was established from a cross between a domesticated breeding line 83A:476 and a wild type P27255 in narrow-leaf lupin (Lupinus angustifolius L.). The parents together with the 89 RILs were subjected to DNA fingerprinting using microsatellite-anchored fragment length polymorphism (MFLP) to rapidly generate DNA markers to construct a linkage map. Five hundred and twenty two unique markers of which 21% were co-dominant, were generated and mapped. Phenotypic data for the domestication traits: mollis (soft seeds), leucospermus (white flower and seed colour); Lentus (reduced pod-shattering), iucundis (low alkaloid), Ku (early flowering) and moustache pattern on seed coats; were included. Three to 7 molecular markers were identified within 5 cM of each of these domestication genes. The anthracnose resistance gene Lanr1 was also mapped. Linkage groups were constructed using MapManager version QTXb20, resulting in 21 linkage groups consisting of 7 or more markers. The total map length was 1543 cM, with an average distance of 3.4 cM between adjacent markers. This is the first published map for a lupin species. The map can be exploited for marker assisted selection for genetic improvement in lupin breeding programs.     

Application of molecular modeling to analysis of inhibition of kinesin motor proteins of the BimC subfamily by monastrol and related compounds

Application of molecular modeling approaches has potential to contribute to rational drug design. These approaches may be especially useful when attempting to elucidate the structural features associated with novel drug targets. In this study, molecular docking and molecular dynamics were applied to studies of inhibition of the human motor protein denoted HsEg5 and other homologues in the BimC subfamily. These proteins are essential for mitosis, so compounds that inhibit their activity may have potential as anticancer therapeutics. The discovery of a small-molecule cell-permeable inhibitor, monastrol, has stimulated research in this area. Interestingly, monastrol is reported to inhibit the human and Xenopus forms of Eg5, but not those from Drosophila and Aspergillus. In this study, homology modeling was used to generate models of the Xenopus, Drosophila, and Aspergillus homologues, using the crystal structure of the human protein in complex with monastrol as a template. A series of known inhibitors was docked into each of the homologues, and the differences in binding energies were consistent with reported experimental data. Molecular dynamics revealed significant changes in the structure of the Aspergillus homologue that may contribute to its relative insensitivity to monastrol and related compounds.     

De-ubiquitinating proteases USP2a and USP2c cause apoptosis by stabilising RIP1

Dynamic ubiquitination impacts on the degradation of proteins by the proteasome as well as on their effects as signalling factors. Of the many cellular responses that are regulated by changes in ubiquitination, apoptosis has garnered special attention. We have found that USP2a and USP2c, two isoforms of the ubiquitin-specific protease USP2, cause cell death upon ectopic expression. We show that both USP2 isoforms can control the ubiquitination status of many proteins but from a panel of potential targets only the protein level of RIP1 was increased by these enzymes. This effect is responsible for the activity of USP2a and USP2c to cause cell death. Both enzymes likewise de-ubiquitinate TRAF2, a ubiquitin-ligase in the TNFR1 complex. Whilst this and the similar sub-cellular localisations of both enzyme isoforms indicate a substantial overlap of activities, inactivation by RNAi revealed that only the knock-down of USP2c resulted in apoptosis, whilst targeting USP2a did not have any consequence on the cells' survival. Consequently, we focussed our studies on USP2a and found that TRAF2 inhibits USP2a's effect on K48- but not on K63-linked ubiquitin chains. Hence, the ratio between USP2a and TRAF2 protein levels determines the cells' sensitivity to cell death.