The Development of the Sexual Stage, Pathogenic Specialization and a Potential Means of Controlling the Urediniophase of Sunflower Rust, 'Puccinia helianthi' schw.

Sunflower rust has been present in Australia for over a century. The uredinial stage is common and is the cause of serious yield losses in commercial sunflower crops. The complete life cycle of this macrocyclic autoecious rust has only rarely been seen in Australia and has not been studied in detail. The importance of the sexual cycle in the epidemiology of sunflower rust in Australia is therefore uncertain. The role of the sexual cycle in the origin of new pathotypes of sunflower rust in Australia is also not known. The purpose of the studies reported in this thesis were to i) investigate and describe aspects of the sexual cycle of 'Puccinia helianthi' in Australia and ii) study a means of controlling the disease through the manipulation of host genes for resistance

Relationships between temperature and latent periods of rust and leaf-spot diseases of groundnut

The effect of temperature on the latent periods of rust, late leaf spot and early leaf spot diseases of groundnut caused by Puccinia arachidis, Phaeoisariopsis personata and Cercospora arachidicola. respectively, was studied. The latent periods (LP) of rust, late leaf spot and early leaf spot ranged from 12-49 days, 13-38 days and 13-39 days, respectively, between 12 C and 33 C An equation relating the rate of pathogen development (1/LP) to temperature was fitted using daily mean temperatures to provide three cardinal temperatures: the minimum (7"m,n), optimum (r^pc), and maximum (Tm,,). T^,^ was about I2°C for rust and about 10°C for the two leaf-spot diseases. Top, for all three diseases was close to 25 C. 7"max was Bl'C for early leaf spot, and extrapolated values for late leaf spot and rust were about 35 and 40°C, respectively

Negative feedback regulation of the ERK1/2 MAPK pathway

The extracellular signal-regulated kinase 1/2 (ERK1/2) mitogen-activated protein kinase (MAPK) signalling pathway regulates many cellular functions, including proliferation, differentiation, and transformation. To reliably convert external stimuli into specific cellular responses and to adapt to environmental circumstances, the pathway must be integrated into the overall signalling activity of the cell. Multiple mechanisms have evolved to perform this role. In this review, we will focus on negative feedback mechanisms and examine how they shape ERK1/2 MAPK signalling. We will first discuss the extensive number of negative feedback loops targeting the different components of the ERK1/2 MAPK cascade, specifically the direct posttranslational modification of pathway components by downstream protein kinases and the induction of de novo gene synthesis of specific pathway inhibitors. We will then evaluate how negative feedback modulates the spatiotemporal signalling dynamics of the ERK1/2 pathway regarding signalling amplitude and duration as well as subcellular localisation. Aberrant ERK1/2 activation results in deregulated proliferation and malignant transformation in model systems and is commonly observed in human tumours. Inhibition of the ERK1/2 pathway thus represents an attractive target for the treatment of malignant tumours with increased ERK1/2 activity. We will, therefore, discuss the effect of ERK1/2 MAPK feedback regulation on cancer treatment and how it contributes to reduced clinical efficacy of therapeutic agents and the development of drug resistance