Our Scientists

The focal point of our project is to develop a practical classroom model to teach classical, molecular, developmental, and biochemical genetics to undergraduates. A rapid-cycling type of Brassica rapa known as FastPlants has been developed into a widely used classroom model by Paul Williams at the University of Wisconsin. Our goal is to develop this B. rapa into a genetic model.

After creating a range of interesting mutants, we will use them as a foundation for creating tools for teaching genetics. For example, dwarf mutants that are deficient in the biosynthesis or sensing of the plant hormone gibberellin provide a great tool to teach biochemical genetics. Albino mutants provide an example of a deleterious recessive mutation that prevents survival to maturity. Multiple mutant loci in a given category provide an opportunity to develop the concept of a complementation test and complementation groups, as well as biochemical pathways. We hope to identify polymorphic markers that can be used to illustrate the molecular genetic concept of using DNA polymorphisms to track genes.

This project will rely heavily on teams of undergraduates (science and education majors) working with graduate students and postdoctoral fellows. The involvement of graduate students and postdoctoral fellows will help to foster a commitment to science education in their future careers. In addition, we are the only group generating mutants in B. rapa, thus undergraduates will be able to explore new scientific territory as well as develop teaching tools and classroom experiments by using these tools. In the later phases of the project, we will introduce these materials into K-12 classrooms.

We will also offer a course that will help foster an understanding of science among undergraduates who are not science majors. A focus of the course will be the dynamic nature of the Earth's history and how that has shaped evolution and vice versa. There will be an emphasis on biochemical evolution and its role in atmospheric change (e.g., the oxygenation of the atmosphere after the evolution of photosynthesis) and the resulting effects on the course of evolution (e.g., the role of oxygen in permitting more complex multicellular organisms to evolve). The overall goal of the course is to engender an appreciation of science within students and to provide them with the tools to distinguish, throughout their future careers, what is real science versus what purports to be, but is not.

Research in the Amasino Lab

One of the most critical aspects of the life cycle of a plant is when flowering is initiated. Many plant species regulate flowering time in response to seasonal cues. One cue that we have studied is exposure to winter cold. Certain plants, for example most biennials, do not initiate flowering unless they have experienced the prolonged cold of winter. This promotion of flowering by prolonged exposure to cold is known as vernalization. Most organisms can sense cold, but plants have evolved the ability to count, at a cellular level, the number of days they have been exposed to cold. This ability is critical to ensure that flowering does not occur after short cold spells in the autumn.

Before our work, “classic” plant physiology studies had shown that vernalization causes the acquisition of the competence to flower, but no molecular details were known. Our work has provided a molecular outline of vernalization-mediated competence in Arabidopsis thaliana. Our genetic analysis of natural variation in the vernalization response led to the identification of two dominant genes that cooperate to confer a vernalization requirement:  FRIGIDA (FRI) and FLOWERING LOCUS C ( FLC). FLC is a potent repressor of flowering that is active in meristems in autumn.

The role of FRI is to elevate autumnal  FLC expression to a level that prevents flowering. During winter, vernalization causes the acquisition of competence by repressing FLC expression. Once FLC is repressed by vernalization, it remains off for the rest of the life cycle after warm conditions return, that is, the repression is epigenetic in the sense that it is mitotically stable in the absence of the inducing signal (cold exposure). In the next generation,  FLC expression is reset to the expressed state. This meiotic resetting is reminiscent of genomic imprinting in mammals. Our recent work has addressed the molecular basis of this epigenetic memory of winter that is manifest as FLC repression. FLC is repressed during vernalization through a series of histone modifications initiated by induction of a gene by prolonged cold, VERNALIZATION INSENSITIVE 3 (VIN3), which encodes a cold-specific component of the plat Polycomb repression complex.

Last updated May 2014