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Frederick Meins


My long-term interest is epigenetic modifications and their role in determination. As a graduate student at Rockefeller University, I decided to work on plants because it was possible to distinguish between epigenetic changes and genetic mutations by genetic analysis of plants regenerated from individual somatic cells. I am particularly fond of work started in the 1970's at Princeton University and the University of Illinois-Urbana that established the existence of cell-heritable determination in plants, overturned the commonly accepted idea that plant cells "forget" their determined state in culture, and led to a mathematical framework for estimating cellular variation rates in tissues. Later we showed certain cultured cells also undergo exceeding rapid epigenetic changes that are then inherited as a Mendelian trait. These findings suggested a plausible explanation for the extreme plasticity of determination in plants and showed that certain epigenetic states in production of growth factors can be transmitted to the next sexual generation.

The 1980s were the start of an exciting period at FMI. The groups of Ingo Potrykus, Barbara Hohn, and Thomas Hohn made pioneering advances in the area of plant genetic transformation. My group focussed on the function of chitinases and Beta-1,3-glucanases in plant innate immunity. Our collaborations with Thomas Boller, who later joined the FMI, and the Ciba-Geigy/ Novartis plant pathology groups led to influential contributions relevant to the evolution of plant gene families, intracellular transport and targeting of proteins, pathogenesis-related signalling pathways, and the function of Beta-1,3-glucanases in viral pathogenesis, cell-to-cell communication, and seed germination.

My interest returned to epigenetics in the late 1980s when we and several other groups discovered what is now called RNA interference (RNAi) in transgenic plants. We discovered that RNAi in plants is an epigenetic form of RNA degradation that persists during somatic development and is transmitted through meiosis. We proposed that this type of epigenetic silencing is maintained by self-sustained production of a sequence-specific "silencing activator" above a critical threshold concentration. Strong support for this threshhold hypothesis came from our finding that siRNAs introduced into cells trigger sustained production of secondary siRNAs from the same target. Rapid progress –particularly after the first small RNAs were cloned in 2000– has established the importance of RNA-silencing in animals and the presence in plants of silencing networks with shared components and overlapping functions. Our most recent work deals with the organization of these networks and the function of microRNAs. For details on this and our earlier work follow the link to "List of Publications".

I retired from FMI in May 2007 after 27 years of continuous support by Ciba-Geigy and then the Novartis Research Foundation. Their blind faith and the remarkable atmosphere, exceptional academic freedom, and resources they provided at FMI allowed me to explore uncharted areas and tackle challenging research problems. I'm particularly proud that many young, talented scientists associated with my group over the years have gone on to establish their own research groups and make important scientific contributions. As an emeritus member, I plan to continue teaching, helping young people, and exploring the "epigenetic landscape" - but with a bit more time to enjoy grandchildren. For a more personal account of my work and the people involved, follow the link to SCIENTIFIC AUTOBIOGRAPHY.
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