Master of Science (M.Sc.)
Genomic imprinting is the preferential expression of one allele over the other. It is an epigenetic phenomenon that occurs in the placentas of mammals and the endosperm of angiosperms. Endosperm, like placentas, is a nutrient rich tissue that supports the growing embryo within the seed. All grains are predominantly composed of this tissue. It is the product of a second fertilization event, resulting in both maternal and paternal alleles. Some alleles are regulated differentially, resulting in imprinted genes. There are both paternally expressed imprinted genes (PEGs) and maternally expressed imprinted genes (MEGs) in the endosperm. In general PEGs tend to have functions that induce the proliferation of endosperm (and the placenta in mammals) and MEGs tend to regulate or limit proliferation. There are many theories on the evolution of imprinting and parent-specific functions in such diverged taxa. Interploidy hybridization systems are often used to study these parent-specific effects. Such systems occur when a diploid is crossed with a polyploid, typically a tetraploid. By switching the parentage, parent specific genome dosage can be altered: if the tetraploid is the mother, then the offspring, or endosperm, has maternal genomic excess, and if the tetraploid is the father, then the endosperm has paternal excess. Maternal excess is typically characterized by endosperm underproliferation and paternal excess is characterized by endosperm overproliferation, as predicted by MEG and PEG functions. While significant progress has been made in genomic imprinting, there is still much unknown. For example, in plants, maternal excess is predicted to be more stable for evolutionary and functional reasons, yet there are many cases where the opposite occurs. By using a system in Mimulus that is both interploidy and interspecies (M. guttatus is diploid and M. luteus is tetraploid) and where paternal excess is favored in offspring viability, we aim to uncover further clues behind the mechanisms and evolutionary drivers of genomic imprinting. Here we show that the paternal excess hybrid suffers from endosperm underproliferation, opposite of what is predicted, and the maternal excess hybrid suffers from complete endosperm and embryo failure. We show that smaller endosperm results in failed or delayed germination. Furthermore, using genomic techniques, we show that M. luteus is genomically dominant in the hybrids regardless of crossing direction, likely interfering with imprinting patterns. We identify new PEGs involved in cellular proliferation. We show an overall paternal bias in M. luteus, which is unexpected and uncommon – potentially suggesting other adaptive drivers in imprinting. We suggest that abnormalities in the hybrids may be due to this genomic dominance and potentially other genetic and developmental differences between the two species that interferes with MEG and PEG roles.
© The Author
Kinser, Taliesin, "Misregulation of Genomic Imprinting Drives Abnormal Seed Development in Hybrid Monkeyflowers (Mimulus)" (2017). Dissertations, Theses, and Masters Projects. Paper 1516639867.