Septins focus cellular growth for host infection by pathogenic fungi

This is the final version of the article. Available from Frontiers Media via the DOI in this record.One of the key challenges faced by microbial pathogens is invasion of host tissue. Fungal pathogens adopt a number of distinct strategies to overcome host cell defenses, including the development of specialized infection structures, the secretion of proteins that manipulate host responses or cellular organization, and the ability to facilitate their own uptake by phagocytic mechanisms. Key to many of these adaptations is the considerable morphogenetic plasticity displayed by pathogenic species. Fungal pathogens can, for example, shift their growth habit between non-polarized spores, or yeast-like cells, and highly polarized hyphal filaments. These polarized filaments can then elaborate differentiated cells, specialized to breach host barriers. Septins play fundamental roles in the ability of diverse fungi to undergo shape changes and organize the F-actin cytoskeleton to facilitate invasive growth. As a consequence, septins are increasingly implicated in fungal pathogenesis, with many septin mutants displaying impairment in their ability to cause diseases of both plants and animals. In this mini-review, we show that a common feature of septin mutants is the emergence of extra polar outgrowths during morphological transitions, such as emergence of germ tubes from conidia or branches from hyphae. We propose that because septins detect and stabilize membrane curvature, they prevent extra polar outgrowths and thereby focus fungal invasive force, allowing substrate invasion.NT is funded by the European Research Council under the European Union's Seventh Framework Programme (FP7/2007-2013)/ERC grant agreement no. 294702 GENBLAST. MM was funded by NSF Grant IOS1051730 from the Developmental Systems Cluster

Harbouring public good mutants within a pathogen population can increase both fitness and virulence

This is the final version of the article. Available from the publisher via the DOI in this record.Existing theory, empirical, clinical and field research all predict that reducing the virulence of individuals within a pathogen population will reduce the overall virulence, rendering disease less severe. Here, we show that this seemingly successful disease management strategy can fail with devastating consequences for infected hosts. We deploy cooperation theory and a novel synthetic system involving the rice blast fungus Magnaporthe oryzae. In vivo infections of rice demonstrate that M. oryzae virulence is enhanced, quite paradoxically, when a public good mutant is present in a population of high-virulence pathogens. We reason that during infection, the fungus engages in multiple cooperative acts to exploit host resources. We establish a multi-trait cooperation model which suggests that the observed failure of the virulence reduction strategy is caused by the interference between different social traits. Multi-trait cooperative interactions are widespread, so we caution against the indiscriminant application of anti-virulence therapy as a disease-management strategy.Natural Environment Research Council NE/E013007/3Natural Environment Research Council Doctoral training grantEngineering and Physical Sciences Research Council Doctoral training grant studentshipEuropean Research Council no. 294702 GENBLASTEuropean Research Council no. 647292 MathModEx

Factors controlling tropospheric O3, OH, NOx, and SO2 over the tropical Pacific during PEM-Tropics B

Observations over the tropical Pacific during the Pacific Exploratory Mission (PEM)-Tropics B experiment (March-April 1999) are analyzed. Concentrations of CO and long-lived nonmethane hydrocarbons in the region are significantly enhanced due to transport of pollutants from northern industrial continents. This pollutant import also enhances moderately O3 concentrations but not NOx concentrations. It therefore tends to depress OH concentrations over the tropical Pacific. These effects contrast to the large enhancements of O3 and NOx concentrations and the moderate increase of OH concentrations due to biomass burning outflow during the PEM-Tropics A experiment (September-October 1996). Observed CH3I concentrations, as in PEM-Tropics A, indicate that convective mass outflux in the middle and upper troposphere is largely independent of altitude over the tropical Pacific. Constraining a one-dimensiohal model with CH3I observations yields a 10-day timescale for convective turnover of the free troposphere, a factor of 2 faster than during PEM-Tropics A. Model simulated HO2, CH2O, H2O2, and CH3OOH concentrations are generally in agreement with observations. However, simulated OH concentrations are lower (∼25%) than observations above 6 km. Whereas models tend to overestimate previous field measurements, simulated HNO3 concentrations during PEM-Tropics B are too low (a factor of 2-4 below 6 km) compared to observations. Budget analyses indicate that chemical production of O3 accounts for only 50% of chemical loss; significant transport of O3 into the region appears to take place within the tropics. Convective transport of CH3OOH enhances the production of HOx and O3 in the upper troposphere, but this effect is offset by HOx loss due to the scavenging of H2O2. Convective transport and scavenging of reactive nitrogen species imply a necessary source of 0.4-1 Tg yr-1 of NOx in the free troposphere (above 4 km) over the tropics. A large fraction of the source could be from marine lightning. Oxidation of DMS transported by convection from the boundary layer could explain the observed free tropospheric SO2 concentrations over the tropical Pacific. This source of DMS due to convection, however, would imply in the model free tropospheric concentrations much higher than observed. The model overestimate cannot be reconciled using recent kinetics measurements of the DMS-OH adduct reaction at low pressures and temperatures and may reflect enhanced OH oxidation of DMS during convection. Copyright 2001 by the American Geophysical Union

Two novel transcriptional regulators are essential for infection-related morphogenesis and pathogenicity of the rice blast fungus Magnaporthe oryzae.

This is the final version of the article. Available from the publisher via the DOI in this record.The cyclic AMP-dependent protein kinase A signaling pathway plays a major role in regulating plant infection by the rice blast fungus Magnaporthe oryzae. Here, we report the identification of two novel genes, MoSOM1 and MoCDTF1, which were discovered in an insertional mutagenesis screen for non-pathogenic mutants of M. oryzae. MoSOM1 or MoCDTF1 are both necessary for development of spores and appressoria by M. oryzae and play roles in cell wall differentiation, regulating melanin pigmentation and cell surface hydrophobicity during spore formation. MoSom1 strongly interacts with MoStu1 (Mstu1), an APSES transcription factor protein, and with MoCdtf1, while also interacting more weakly with the catalytic subunit of protein kinase A (CpkA) in yeast two hybrid assays. Furthermore, the expression levels of MoSOM1 and MoCDTF1 were significantly reduced in both Δmac1 and ΔcpkA mutants, consistent with regulation by the cAMP/PKA signaling pathway. MoSom1-GFP and MoCdtf1-GFP fusion proteins localized to the nucleus of fungal cells. Site-directed mutagenesis confirmed that nuclear localization signal sequences in MoSom1 and MoCdtf1 are essential for their sub-cellular localization and biological functions. Transcriptional profiling revealed major changes in gene expression associated with loss of MoSOM1 during infection-related development. We conclude that MoSom1 and MoCdtf1 functions downstream of the cAMP/PKA signaling pathway and are novel transcriptional regulators associated with cellular differentiation during plant infection by the rice blast fungus.Funding: This work was supported by National Key Basic Research and Development Program of China (2012CB114002), by Program for Changjiang Scholars and Innovative Research Team in University (IRT0943), by the Natural Science Foundation of China (Grant Nos. 30970129 and 31071648) and the Doctoral Fund of Ministry of Education of China (20100101110097) to ZW