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Show COLLEGE OF SCIENCE Leslie Sieburth 66 DOES THE BPS SIGNAL REPRESS WUSCHEL BY ALTERING ITS EPIGENETIC STATE? WALLIE Kanishka (Leslie Sieburth) Department of Biology University of Utah Background -Signaling between cells is a fundamental requirement for normal development in plants,as plant cells are unable to migrate, and because they are sessile, they respond to changes in the environment. Understanding how growth of a plant's shoot system is regulated is important foragricultural productivity. In plants, the WUSCHEL (WUS) gene is required for maintaining stem cell populations in the shoot and floral meristems. W U S is modified epigenetically, and these modifications affect its regulated expression. Epigenetic changes are modifications to genes that do not change the nucleotide sequence. Rather, epigenetic changes modify the structure of D N A (by methylating C and A bases), or modify the structure of core histones (by methylating or acetylating their tails). S o m e epigenetic modifications reduce gene expression, for example by inhibiting the binding of transcription factors to DNA. Other modification enhance gene expression, for example by promoting the binding of transcription factors. Research in the Sieburth lab revealed that the roots are capable of synthesizing the bps signal, which stops shoot growth. This regulation of shoot growth occurs through down-regulation of W U S expression. Hypothesis - My research tests the hypothesis that the bps signal down-regulates WUS expression using an epigenetic mechanism. Approaches -I am using a genetic approach to test whether DNA methylation or histone modifications are required for bps signal regulation of W U S expression.I a m using three mutants with defects in placing repressive epigenetic marks on chromatin. If the bps signal uses any of these three pathways to shut down W U S expression, then the double mutant is expected to be incapable of shutting down W U S expression and will produce a normal-appearing shoot apical meristem. METHYLTRANSFERASE 1 (MET1), encodes the primary D N A methylase, and I a m generating bpsl metl double mutants.The Arabidopsis CURLYLEAF (CLF) gene encodes a Polycomb group protein which is responsible for placing repressive methylation on histones, and I a m generating bpsl clfdouble mutants. The PICKLE (PKL) gene encodes a histone deacety-lase, which removes the histone acetylation that is associated with active chromatin, and I a m generating bpsl pkldouble mutants. F2 plants from each cross will be examined to determine whether the double mutant restores stem cell maintenance; this will be done using a compound microscope. |