Virginia Walbot
Academic Appointments
- Professor, Biology (School of Humanities and Sciences)
- Member, Bio-X
Key Documents
Contact Information
- Academic Offices
Personal Information Email Tel (650) 723-2007 Tel (650) 723-2227Alternate Contact Alexandra Bloom Administrative Assistant Email Tel Work 650-723-2007
Professional Overview
Administrative Appointments
- Elected to the Steering Committee of the Faculty Senate, Stanford (2009 - 2011)
- Elected to Faculty Senate, Stanford (2009 - 2011)
- Elected to Faculty Senate, Stanford (1999 - 2001)
- Committee on Committees, Stanford (2000 - 2001)
- Committee on Research, Stanford (2003 - 2005)
Honors and Awards
- Cooresponding Member, Mexican Academy of Sciences (2004)
- Hageman Lectureship, Kansas State University (2001)
- Joan V. Wood Lectureship, Indiana University (1999)
- Explorer Award, National Geographic Society (1998)
- Eppley Award, Eppley Foundation (1993)
- Fellow, Guggenheim Foundation (1987)
Professional Education
| Postdoc: | Univ. Georgia, Biochemistry (1975) |
| Ph.D.: | Yale University, Biology (1972) |
| M. Phil.: | Yale University, Biology (1969) |
| A. B.: | Stanford, Biology (1967) |
Graduate & Fellowship Program Affiliations
Community and International Work
- UV-B Irradiation, Stanford
- Corn cancer caused by Ustilago maydis, Stanford CA
- Cell Fate Acquisition, Cal Poly and Stanford
- DNA Methylation Society, International
Internet Links
Scientific Focus
Current Research Interests
Research Interests
My central interest is the mechanisms that create allelic diversity and modulate genome stability in plants. The key features of plant development are that the body plan is indefinite, with continual stem cell activity producing new organs, and that there is an alternation of generations in which the phenotypes of haploid cells are determined mainly by their genotype. These life cycle features allow somatic and gametic selection to operate more stringently than in complex animals with a fixed body plan and in animal gametes. Our primary focus has been the regulation of MuDR/Mu transposable elements in the context of the maize life cycle. Our most recent projects involve analysis of a mutants in cell fate specification in maize anthers. The anther locules have just 5 cell types, including the cells that ultimately undergo meiosis. Using a panel of male sterile mutants, transcriptome profiling, proteomics, and genetic analysis we are defining how these cells acquire their fates, and then maintain them. As different cell types support different Mu transposon activities, we expect to uncover the host regulation of the transposons through this study. We are particularly interested in late signaling events within the anther to specify cell fate and have both mutants and novel candidate protein signal molecules to test.
MuDR/Mu elements exhibit two forms of developmental regulation: very late activation and a difference in transpositional outcome in somatic and pre-germinal cells. Mu elements are active only during terminal cell divisions of tissue development, a feature that is post-transcriptionally regulated, because the MURA transposase and MURB helper proteins encoded by MuDR are ubiquitously present. In the soma, activation results in element excision (cut & paste or "cut only" transposition), however, in pre-meiotic cells and in gametes, activation results in insertion without element excision (replicative transposition or "cut and paste" with faithful gap-repair replacement). The ability to change transpositional outcomes is a unique attribute of this eukaryotic transposon. Using a combination of genetic analysis and construction of transgenic plants expressing specific forms of MURA and MURB and modified terminal inverted repeats we are elucidating the cis and trans requirements for developmental regulation. We have identified two MURA transposases that result from alternative splicing of the third intron; both are capable of excision without insertion. We proved that the MURB product of MuDR is required for insertion. We identified a third MURA transposase resulting from alternative splicing of the first intron and frameshift translation as the best candidate for the net replicative transposition; transgenic maize expressing this protein are currently being analyzed.
Almost inevitably MuDR becomes transcriptionally silenced in lines not selected for maintenance of transposition. In effect, the host wins, converting the numerous MuDR/Mu elements to stable components of the genome. We have elucidated contributions to post-transcriptional regulation exerted by natural antisense RNA and by transcripts from homologs of MuDR already present in the genome. Transcriptionally silenced and methylated MuDR elements can reactivate spontaneously at a very low frequency.
Publications
- Hypoxia triggers meiotic fate acquisition in maize. Science. 2012; (6092): 345-8
- Emergence and patterning of the five cell types of the Zea mays anther locule. Dev Biol. 2011; (1): 32-49
- Global transcriptome analysis of two ameiotic1 alleles in maize anthers: defining steps in meiotic entry and progression through prophase I. BMC Plant Biol. 2011: 120
- Maize host requirements for Ustilago maydis tumor induction. Sex Plant Reprod. 2010; (1): 1-13
- Maize tumors caused by Ustilago maydis require organ-specific genes in host and pathogen. Science. 2010; (5974): 89-92
- The male sterile 8 mutation of maize disrupts the temporal progression of the transcriptome and results in the mis-regulation of metabolic functions. Plant J. 2010; (6): 939-51
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