University of Kentucky

Poster Title

Seed Maturation Protein

Presenter Information

Taylor Lloyd, University of Kentucky

Institution

University of Kentucky

Abstract

My project was a continuation on previous work by my Principal Investigator, Dr. A. Bruce Downie, UK Horticulture. It had previously been discovered that the gene At3g12960 product, Seed Maturation Protein (SMP), was susceptible to aging damage as isoaspartate accumulation. Also, the aging damage was found to be targeted by the enzyme, PIMT, which repaired the damage. Further interest into why the seed found this protein to be significant for repair spurred my project. My project was to identify the phenotype for the SMP gene through work with a mutant, smp1-3. In addition to the identifying the phenotype, my work encompassed confirming the cause for the phenotype to be the gene of interest through sequencing and confirmation of the “knocked-down” expression of the protein. The gene was found to control the seeds behavior following temperature shock. When the Wild Type (WT) was compared to the smp1-3 knockdown, it was seen that the mutant lacked the self-preservation technique of waiting several days following temperature shock. Instead of waiting to ensure the temperature was not going to change again, the mutant germinated several days earlier. Empirically, I proved that it was the SMP gene, which controlled this behavior by testing the location of the transposon (Maize Ac). The transposon prevented the functional protein responsible for the seeds behavior to be made. It was shown that no other inserted transposons caused the mutation and provided us with a clear understanding of the role of this gene in the germination process.

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Seed Maturation Protein

My project was a continuation on previous work by my Principal Investigator, Dr. A. Bruce Downie, UK Horticulture. It had previously been discovered that the gene At3g12960 product, Seed Maturation Protein (SMP), was susceptible to aging damage as isoaspartate accumulation. Also, the aging damage was found to be targeted by the enzyme, PIMT, which repaired the damage. Further interest into why the seed found this protein to be significant for repair spurred my project. My project was to identify the phenotype for the SMP gene through work with a mutant, smp1-3. In addition to the identifying the phenotype, my work encompassed confirming the cause for the phenotype to be the gene of interest through sequencing and confirmation of the “knocked-down” expression of the protein. The gene was found to control the seeds behavior following temperature shock. When the Wild Type (WT) was compared to the smp1-3 knockdown, it was seen that the mutant lacked the self-preservation technique of waiting several days following temperature shock. Instead of waiting to ensure the temperature was not going to change again, the mutant germinated several days earlier. Empirically, I proved that it was the SMP gene, which controlled this behavior by testing the location of the transposon (Maize Ac). The transposon prevented the functional protein responsible for the seeds behavior to be made. It was shown that no other inserted transposons caused the mutation and provided us with a clear understanding of the role of this gene in the germination process.