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The Max Planck Institute for Plant Breeding Research was originally founded in Müncheberg, Germany in 1928 as part of the Kaiser-Wilhelm-Gesellschaft. The founding Director, Erwin Baur, initiated breeding programmes with fruits and berries, as well as basic research on Antirrhinum majus and the domestication of lupins. After the Second World War, the Institute moved west to Voldagsen, and was relocated to new buildings on the present site in Cologne in 1955. The modern era of the Institute began in 1978 with the appointment of Jeff Schell and the development of plant transformation technologies and plant molecular genetics. The focus on molecular genetics was extended in 1980 with the appointment of Heinz Saedler. The appointment in 1983 of Klaus Hahlbrock broadened the expertise of the Institute in the area of plant biochemistry, and the arrival of Francesco Salamini in 1985 added a focus on crop genetics. During the period 1978-1990, the Institute was greatly expanded and new buildings were constructed for the departments led by Schell, Hahlbrock and Salamini, in addition to a new lecture hall and the Max Delbrück Laboratory building that housed independent research groups over a period of 10 years.A new generation of Directors was appointed from 2000 with the approaching retirements of Klaus Hahlbrock and Jeff Schell. Paul Schulze-Lefert and George Coupland were appointed in 2000 and 2001, respectively, and Maarten Koornneef arrived three years later upon the retirement of Francesco Salamini. The new scientific departments brought a strong focus on utilising model species to understand the regulatory principles and molecular mechanisms underlying selected traits. The longer-term aim is to translate these discoveries to breeding programmes through the development of rational breeding concepts. The arrival of a new generation of Directors also required modernisation of the infrastructure. So far, this has involved complete refurbishment of the building that houses the Plant Developmental Biology laboratory , construction of a new guesthouse and library , planning of new buildings for the administration and technical workshops , as well as a new laboratory building completed in May 2012. The new laboratory building includes a section that links all three scientific departments, offices and the Bioinformatics Research Group.CurrentlyTemplate:When? the Institute hosts three scientific departments: Department of Plant Developmental Biology , Department of Plant Breeding and Genetics and Department of Plant Microbe Interactions . Wikipedia.


Kemen E.,Max Planck Institute for Plant Breeding Research
Current Opinion in Plant Biology | Year: 2014

Microbial organisms sharing habitats aim for maximum fitness that they can only reach by collaboration. Developing stable networks within communities are crucial and can be achieved by exchanging common goods and genes that benefit the community. Only recently was it shown that horizontal gene transfer is not only common between prokaryotes but also into eukaryotic organisms such as fungi and oomycetes benefiting communal stability. Eukaryotic plant symbionts and pathogens coevolve with the plant microbiome and can acquire the ability to communicate or even collaborate, facilitating communal host colonization. Understanding communal infection will lead to a mechanistic understanding in how new hosts can be colonized under natural conditions and how we can counteract. © 2014. Source


Schmidt S.M.,University of Amsterdam | Panstruga R.,Max Planck Institute for Plant Breeding Research
Current Opinion in Plant Biology | Year: 2011

Members of the kingdom fungi comprise numerous plant pathogens, including the causal agents of many agriculturally relevant plant diseases such as rust, powdery mildew, rice blast and cereal head blight. Data from recent sequencing projects provide deep insight into the genomes of a range of fungi that infect different organs of monocotyledonous or dicotyledonous hosts and that have diverse pathogenic lifestyles. These studies have revealed that, similar to sequenced phytopathogenic oomycetes, these plant parasites possess very plastic and dynamic genomes, which typically encode several hundred candidate secreted effector proteins that can be highly divergent even among related species. A new insight is the presence of lineage-specific genes on mobile and partly dispensable chromosomes that are transferred intraspecifically and possibly interspecifically, thereby constituting pathogenicity and host range determinants. Convergent lifestyle-specific adaptations have shaped the parasite genomes to maximize pathogenic success according to the different infection strategies employed. © 2011 Elsevier Ltd. Source


Kombrink E.,Max Planck Institute for Plant Breeding Research
Planta | Year: 2012

Jasmonates are lipid-derived compounds that act as signals in plant stress responses and developmental processes. Enzymes participating in biosynthesis of jasmonic acid (JA) and components of JA signaling have been extensively characterized by biochemical and molecular-genetic tools. Mutants have helped to define the pathway for synthesis of jasmonoyl-l-isoleucine (JA-Ile), the bioactive form of JA, and to identify the F-box protein COI1 as central regulatory unit. Details on the molecular mechanism of JA signaling were recently unraveled by the discovery of JAZ proteins that together with the adaptor protein NINJA and the general co-repressor TOPLESS form a transcriptional repressor complex. The current model of JA perception and signaling implies the SCFCOI1 complex operating as E3 ubiquitin ligase that upon binding of JA-Ile targets JAZ proteins for degradation by the 26S proteasome pathway, thereby allowing MYC2 and other transcription factors to activate gene expression. Chemical strategies, as integral part of jasmonate research, have helped the establishment of structure-activity relationships and the discovery of (+)-7-iso-JA-l-Ile as the major bioactive form of the hormone. The transient nature of its accumulation highlights the need to understand catabolism and inactivation of JA-Ile and recent studies indicate that oxidation of JA-Ile by cytochrome P450 monooxygenase is the major mechanism for turning JA signaling off. Plants contain numerous JA metabolites, which may have pronounced and differential bioactivity. A major challenge in the field of plant lipid signaling is to identify the cognate receptors and modes of action of these bioactive jasmonates/oxylipins. © 2012 Springer-Verlag. Source


Garcia A.V.,Max Planck Institute for Plant Breeding Research
PLoS pathogens | Year: 2010

An important layer of plant innate immunity to host-adapted pathogens is conferred by intracellular nucleotide-binding/oligomerization domain-leucine rich repeat (NB-LRR) receptors recognizing specific microbial effectors. Signaling from activated receptors of the TIR (Toll/Interleukin-1 Receptor)-NB-LRR class converges on the nucleo-cytoplasmic immune regulator EDS1 (Enhanced Disease Susceptibility1). In this report we show that a receptor-stimulated increase in accumulation of nuclear EDS1 precedes or coincides with the EDS1-dependent induction and repression of defense-related genes. EDS1 is capable of nuclear transport receptor-mediated shuttling between the cytoplasm and nucleus. By enhancing EDS1 export from inside nuclei (through attachment of an additional nuclear export sequence (NES)) or conditionally releasing EDS1 to the nucleus (by fusion to a glucocorticoid receptor (GR)) in transgenic Arabidopsis we establish that the EDS1 nuclear pool is essential for resistance to biotrophic and hemi-biotrophic pathogens and for transcriptional reprogramming. Evidence points to post-transcriptional processes regulating receptor-triggered accumulation of EDS1 in nuclei. Changes in nuclear EDS1 levels become equilibrated with the cytoplasmic EDS1 pool and cytoplasmic EDS1 is needed for complete resistance and restriction of host cell death at infection sites. We propose that coordinated nuclear and cytoplasmic activities of EDS1 enable the plant to mount an appropriately balanced immune response to pathogen attack. Source


Pecinka A.,Max Planck Institute for Plant Breeding Research
Trends in plant science | Year: 2013

Transcriptional gene silencing (TGS) is an epigenetic mechanism that suppresses the activity of repetitive DNA elements via accumulation of repressive chromatin marks. We discuss natural variation in TGS, with a particular focus on cases that affect the function of protein-coding genes and lead to developmental or physiological changes. Comparison of the examples described has revealed that most natural variation is associated with genetic determinants, such as gene rearrangements, inverted repeats, and transposon insertions that triggered TGS. Recent technical advances have enabled the study of epigenetic natural variation at a whole-genome scale and revealed patterns of inter- and intraspecific epigenetic variation. Future studies exploring non-model species may reveal species-specific evolutionary adaptations at the level of chromatin configuration. Copyright © 2013 Elsevier Ltd. All rights reserved. Source

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