Seed development in Arabidopsis thaliana
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The evolutionary success of seed plants can be attributed in part to their ability to produce a resilient structure, the seed, which allows the embryo to suspend development and only resume its life cycle once suitable environmental conditions are met. Seed formation not only significantly increases embryo survivability, but also allows the embryo to across extraordinary distances, all the while lying dormant. Seed plants have thus been able to occupy and adapt to almost every terrestrial habitat on the planet. Mature seeds are desiccated, and contain storage products that are to be used by the seedling after germination. These properties are the outcome of the embryo maturation program. A complex network is involved in timing maturation during embryo development. Several “master regulators” (the “LEC genes”) are required for the induction of the maturation program in mid-embryogenesis, but the mechanisms that repress this program during early embryogenesis are less clear. Previous research in Dr. Jenik’s lab identified several genes in Arabidopsis thaliana (DCL1, ASIL1, ASIL2, HDA6) that are required to prevent the early onset of the maturation program (Willmann et al., 2011). The genes that are the focus of this project are ASIL1 (ARABIDOPSIS 6B-INTERACTING PROTEIN1-LIKE1) and its closest paralog ASIL2, which encode proteins of the plant-specific trihelix transcription factor family. ASIL1 has been shown to repress the maturation program both in the seedling and in the embryo (Gao et al., 2009, 2011). I seek to characterize the roles of ASIL1 and ASIL2 during early seed development, first by characterizing the expression of two of the “LEC genes” (LEAFY COTYLEDON2 [LEC2] and FUSCA3 [FUS3]) in wild type and mutant embryos using reporter genes. Early analyses indicate that the seeds of asil1-1, asil2-1, and asil1-1 asil2-1 double mutants show early expression of LEC2. I also study the regulation of ASIL1 and ASIL2 throughout embryogenesis by generating deletions in the promoter regions of both genes and fusing them to reporter genes. After studying five such constructs of ASIL1, I have identified several putative regulatory sequences both in the promoter region, as well as in the 5’ UTR of the gene.
Franklin and Marshall College Archives, Undergraduate Honors Thesis 2015
- F&M Theses Collection