Michael Freeling

University of California, Berkeley


Election Year: 1994
Primary Section: 62, Plant, Soil, and Microbial Sciences
Membership Type: Member

Biosketch

Michael Freeling, U.S. geneticist. Freeling (Mike) received his PhD in 1973 from Indiana University with Drew Schwartz (Major Prof.), Marcus Rhoades, Carlos Williams, and Robert Briggs. He immediately became a professor at UC Berkeley, where he remains, teaching both nonmajors and graduate students. He has mentored 25 doctoral students, 42 postdocs, and was elected to the US National Academy of Sciences in 1994. The lab’s early work on gene regulation, anaerobic genes and transposons changed to developmental genetics, especially of leaves; from 1999 through 2014, transposon research was lead by PI Damon Lisch. By 2003, Freeling himself had switched his energies to plant comparative genomics and understanding evolutionary trends: see his Google citation index, and his lab webpage (http://Freelinglab.berkeley.edu) and his lab's on‐line comparative genomics toolbox: CoGe (now public at iPlant: https://genomevolution.org/CoGe/).

Research Interests

There are two research areas in our laboratory.The first is the molecular genetics of the maize leaf and the repeating segment from which it originates. The second is the evolution and genetics of the ligule in grasses. In general, we induce or obtain mutants, describe their phenotypes, tag, clone, and sequence the cDNA and genomic, and then begin to organize gene functions into paths or nets to obtain a better idea of how genes regulate early leaf development. A few homeodomain genes affecting embryo, meristem, and leaf have been sequenced, a gene involved in vegetative phase change has been cloned, and genes that provide identity to a domain of phytomer (segment) has been tagged. Several other mutants of even greater interest are in some stage of characterization. Our maize system is particularly fit to study how development is timed and the meaning of "heterochronic" mutants. The later genes act in development, the easier it is to analyze their functions. The induction of the ligule happens within the leaf primordium itself, and is a relatively late organogenic event. We have characterized by phenotype, cloned and sequenced each of the two genes specifically necessary to specify the ligular region that bisects a typical leaf. Both are transcription factors (bZIP and SBP classes), although one specifies noncell-autonomous phenotype early and the other acts cell-autonomously. We are understanding rapidly this signal emission, cell-cell transmission-reception, transduction and resignalling pathway to ligule induction. We have preliminary evidence for the involvement of a particular protein receptor kinase and are trying to fill-in the gene regulatory gaps using both molecular biology and suppresser screens. At present, perhaps our most ambitious experiments involve swapping genes between maize and rice as one way to deduce the molecular basis for morphological and histological differences between organs. We are particularly excited about the mutant phenotype Narrow Sheath, encoded by two genes that behave as duplicate factors. The Narrow Sheath leaf is the skinny one; it is missing the clear marginal area in the diagram. Both genes are tagged with Mu insertions and should be cloned soon. A NS leaf fails to identify organ identities in a domain of segment defined by being opposite to the midvein of the leaf.

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