Ozone-induced signaling in Arabidopsis thaliana

Tropospheric ozone (O3) is one of the most common air pollutants in industrialized countries, and an increasing problem in rapidly industrialising and developing countries in Asia, Africa and South America. Elevated concentrations of tropospheric O3 can lead to decrease in photosynthesis rate and therefore affect the normal metabolism, growth and seed production. Acute and high O3 episodes can lead to extensive damage leading to dead tissue in plants. Thus, O3 derived growth defects can lead to reduction in crop yield thereby leading to economical losses. Despite the extensive research on this area, many questions remain open on how these processes are controlled. In this study, the stress-induced signaling routes and the components involved were elucidated in more detail starting from visual damage to changes in gene expression, signaling routes and plant hormone interactions that are involved in O3-induced cell death. In order to elucidate O3-induced responses in Arabidopsis, mitogen-activated protein kinase (MAPK) signaling was studied using different hormonal signaling mutants. MAPKs were activated at the beginning of the O3 exposure. The activity of MAPKs, which were identified as AtMPK3 and AtMPK6, reached the maximum at 1 and 2 hours after the start of the exposure, respectively. The activity decreased back to clean air levels at 8 hours after the start of the exposure. Both AtMPK3 and AtMPK6 were translocated to nucleus at the beginning of the O3 exposure where they most likely affect gene expression. Differences were seen between different hormonal signaling mutants. Functional SA signaling was shown to be needed for the full protein levels and activation of AtMPK3. In addition, AtMPK3 and AtMPK6 activation was not dependent on ethylene signaling. Finally, jasmonic acid was also shown to have an impact on AtMPK3 protein levels and AtMPK3 activity. To further study O3-induced cell death, an earlier isolated O3 sensitive Arabidopsis mutant rcd1 was mapped, cloned and further characterized. RCD1 was shown to encode a gene with WWE and ADP-ribosylation domains known to be involved in protein-protein interactions and cell signaling. rcd1 was shown to be involved in many processes including hormonal signaling and regulation of stress-responsive genes. rcd1 is sensitive against O3 and apoplastic superoxide, but tolerant against paraquat that produces superoxide in chloroplast. rcd1 is also partially insensitive to glucose and has alterations in hormone responses. These alterations are seen as ABA insensitivity, reduced jasmonic acid sensitivity and reduced ethylene sensitivity. All these features suggest that RCD1 acts as an integrative node in hormonal signaling and it is involved in the hormonal regulation of several specific stress-responsive genes. Further studies with the rcd1 mutant showed that it exhibits the classical features of programmed cell death, PCD, in response to O3. These include nuclear shrinkage, chromatin condensation, nuclear DNA degradation, cytosol vesiculation and accumulation of phenolic compounds and eventually patches of HR-like lesions. rcd1 was found to produce extensive amount of salicylic acid and jasmonic acid in response to O3. Double mutant studies showed that SA independent and dependent processes were involved in the O3-induced PCD in rcd1 and that increased sensitivity against JA led to increased sensitivity against O3. Furthermore, rcd1 had alterations in MAPK signature that resembled changes that were previously seen in mutants defective in SA and JA signaling. Nitric oxide accumulation and its impact on O3-induced cell death were also studied. Transient accumulation of NO was seen at the beginning of the O3 exposure, and during late time points, NO accumulation coincided with the HR-like lesions. NO was shown to modify defense gene expression, such as, SA and ethylene biosynthetic genes. Furthermore, rcd1 was shown to produce more NO in control conditions. In conclusion, NO was shown to be involved in O3-induced signaling leading to attenuation of SA biosynthesis and other defense related genes.

Relationships in food chains: an empirical examination of trust, commitment and communication

This report derives from the EU funded research project “Key Factors Influencing Economic Relationships and Communication in European Food Chains” (FOODCOMM). The research consortium consisted of the following organisations: University of Bonn (UNI BONN), Department of Agricultural and Food Marketing Research (overall project co-ordination); Institute of Agricultural Development in Central and Eastern Europe (IAMO), Department for Agricultural Markets, Marketing and World Agricultural Trade, Halle (Saale), Germany; University of Helsinki, Ruralia Institute Seinäjoki Unit, Finland; Scottish Agricultural College (SAC), Food Marketing Research Team - Land Economy Research Group, Edinburgh and Aberdeen; Ashtown Food Research Centre (AFRC), Teagasc, Food Marketing Unit, Dublin; Institute of Agricultural & Food Economics (IAFE), Department of Market Analysis and Food Processing, Warsaw and Government of Aragon, Center for Agro-Food Research and Technology (CITA), Zaragoza, Spain. The aim of the FOODCOMM project was to examine the role (prevalence, necessity and significance) of economic relationships in selected European food chains and to identify the economic, social and cultural factors which influence co-ordination within these chains. The research project considered meat and cereal commodities in six different European countries (Finland, Germany, Ireland, Poland, Spain, UK/Scotland) and was commissioned against a background of changing European food markets. The research project as a whole consisted of seven different work packages. This report presents the results of qualitative research conducted for work package 5 (WP5) in the pig meat and rye bread chains in Finland. Ruralia Institute would like to give special thanks for all the individuals and companies that kindly gave up their time to take part in the study. Their input has been invaluable to the project. The contribution of research assistant Sanna-Helena Rantala was significant in the data gathering. FOODCOMM project was coordinated by the University of Bonn, Department of Agricultural and Food Market Research. Special thanks especially to Professor Monika Hartmann for acting as the project leader of FOODCOMM.