Bio


Jennifer Stonaker is an advanced lecturer in the Program in Writing and Rhetoric. She has a PhD in plant biology from UC Berkeley, where she employed genetic and bioinformatic tools to study gene regulation in maize. Her current research focuses on science communication and writing pedagogy, particularly in how electronic portfolios and reflection can promote learning. She is also interested in science outreach, having previously worked as a science instructor and curriculum developer at the Tech Museum in San Jose and the Cal Academy of Sciences in San Francisco.

Academic Appointments


  • PWR Advanced Lecturer, Writing and Rhetoric Studies

Administrative Appointments


  • Coordinator of Pedagogical Technology, Program in Writing and Rhetoric (2021 - Present)
  • Co-chair, Lecturer Affairs Committee, Program in Writing and Rhetoric (2021 - 2022)
  • Writing Specialist, Program in Human Biology (2019 - 2020)
  • Coordinator, Notation in Science Communication (2014 - 2018)
  • Co-chair, Curriculum Committee, Program in Writing and Rhetoric (2016 - 2018)

Professional Education


  • PhD, University of California, Berkeley, Plant Biology and Genetics
  • BS, University of Texas at Austin, Molecular Biology
  • BA, University of Texas at Austin, Plan II Honors

Current Research and Scholarly Interests


SPECIALIZATION: Electronic Portfolios; Science Communication; Science Storytelling

All Publications


  • Science Communication across Disciplines: Reflecting on STEM Identity Building through Notation in Science Communication ePortfolios Across the Disciplines: A Journal of Language, Learning and Academic Writing Alfano, C., Polk, E., Stonaker, J. 2023; 20 (3/4)
  • Metacognition across the Curriculum: Building Capstone ePortfolios in Stanford University's Notation in Science Communication ePortfolio as Curriculum Stonaker, J., Druckman, J., Carpenter, R., Chen, H. L. edited by Yancey, K. B. 2019
  • required to maintain repression2 is a novel protein that facilitates locus-specific paramutation in maize. The Plant cell Barbour, J. R., Liao, I. T., Stonaker, J. L., Lim, J. P., Lee, C. C., Parkinson, S. E., Kermicle, J., Simon, S. A., Meyers, B. C., Williams-Carrier, R., Barkan, A., Hollick, J. B. 2012; 24 (5): 1761-75

    Abstract

    Meiotically heritable epigenetic changes in gene regulation known as paramutations are facilitated by poorly understood trans-homolog interactions. Mutations affecting paramutations in maize (Zea mays) identify components required for the accumulation of 24-nucleotide RNAs. Some of these components have Arabidopsis thaliana orthologs that are part of an RNA-directed DNA methylation (RdDM) pathway. It remains unclear if small RNAs actually mediate paramutations and whether the maize-specific molecules identified to date define a mechanism distinct from RdDM. Here, we identify a novel protein required for paramutation at the maize purple plant1 locus. This required to maintain repression2 (RMR2) protein represents the founding member of a plant-specific clade of predicted proteins. We show that RMR2 is required for transcriptional repression at the Pl1-Rhoades haplotype, for accumulation of 24-nucleotide RNA species, and for maintenance of a 5-methylcytosine pattern distinct from that maintained by RNA polymerase IV. Genetic tests indicate that RMR2 is not required for paramutation occurring at the red1 locus. These results distinguish the paramutation-type mechanisms operating at specific haplotypes. The RMR2 clade of proteins provides a new entry point for understanding the diversity of epigenomic control operating in higher plants.

    View details for DOI 10.1105/tpc.112.097618

    View details for PubMedID 22562610

    View details for PubMedCentralID PMC3442568

  • Diversity of Pol IV function is defined by mutations at the maize rmr7 locus. PLoS genetics Stonaker, J. L., Lim, J. P., Erhard, K. F., Hollick, J. B. 2009; 5 (11): e1000706

    Abstract

    Mutations affecting the heritable maintenance of epigenetic states in maize identify multiple small RNA biogenesis factors including NRPD1, the largest subunit of the presumed maize Pol IV holoenzyme. Here we show that mutations defining the required to maintain repression7 locus identify a second RNA polymerase subunit related to Arabidopsis NRPD2a, the sole second largest subunit shared between Arabidopsis Pol IV and Pol V. A phylogenetic analysis shows that, in contrast to representative eudicots, grasses have retained duplicate loci capable of producing functional NRPD2-like proteins, which is indicative of increased RNA polymerase diversity in grasses relative to eudicots. Together with comparisons of rmr7 mutant plant phenotypes and their effects on the maintenance of epigenetic states with parallel analyses of NRPD1 defects, our results imply that maize utilizes multiple functional NRPD2-like proteins. Despite the observation that RMR7/NRPD2, like NRPD1, is required for the accumulation of most siRNAs, our data indicate that different Pol IV isoforms play distinct roles in the maintenance of meiotically-heritable epigenetic information in the grasses.

    View details for DOI 10.1371/journal.pgen.1000706

    View details for PubMedID 19936246

    View details for PubMedCentralID PMC2775721

  • RNA polymerase IV functions in paramutation in Zea mays. Science (New York, N.Y.) Erhard, K. F., Stonaker, J. L., Parkinson, S. E., Lim, J. P., Hale, C. J., Hollick, J. B. 2009; 323 (5918): 1201-5

    Abstract

    Plants have distinct RNA polymerase complexes (Pol IV and Pol V) with largely unknown roles in maintaining small RNA-associated gene silencing. Curiously, the eudicot Arabidopsis thaliana is not affected when either function is lost. By use of mutation selection and positional cloning, we showed that the largest subunit of the presumed maize Pol IV is involved in paramutation, an inherited epigenetic change facilitated by an interaction between two alleles, as well as normal maize development. Bioinformatics analyses and nuclear run-on transcription assays indicate that Pol IV does not engage in the efficient RNA synthesis typical of the three major eukaryotic DNA-dependent RNA polymerases. These results indicate that Pol IV employs abnormal RNA polymerase activities to achieve genome-wide silencing and that its absence affects both maize development and heritable epigenetic changes.

    View details for DOI 10.1126/science.1164508

    View details for PubMedID 19251626

  • A novel Snf2 protein maintains trans-generational regulatory states established by paramutation in maize. PLoS biology Hale, C. J., Stonaker, J. L., Gross, S. M., Hollick, J. B. 2007; 5 (10): e275

    Abstract

    Paramutations represent heritable epigenetic alterations that cause departures from Mendelian inheritance. While the mechanism responsible is largely unknown, recent results in both mouse and maize suggest paramutations are correlated with RNA molecules capable of affecting changes in gene expression patterns. In maize, multiple required to maintain repression (rmr) loci stabilize these paramutant states. Here we show rmr1 encodes a novel Snf2 protein that affects both small RNA accumulation and cytosine methylation of a proximal transposon fragment at the Pl1-Rhoades allele. However, these cytosine methylation differences do not define the various epigenetic states associated with paramutations. Pedigree analyses also show RMR1 does not mediate the allelic interactions that typically establish paramutations. Strikingly, our mutant analyses show that Pl1-Rhoades RNA transcript levels are altered independently of transcription rates, implicating a post-transcriptional level of RMR1 action. These results suggest the RNA component of maize paramutation maintains small heterochromatic-like domains that can affect, via the activity of a Snf2 protein, the stability of nascent transcripts from adjacent genes by way of a cotranscriptional repression process. These findings highlight a mechanism by which alleles of endogenous loci can acquire novel expression patterns that are meiotically transmissible.

    View details for DOI 10.1371/journal.pbio.0050275

    View details for PubMedID 17941719

    View details for PubMedCentralID PMC2020503