| dc.description.abstract |
<p>The earth is home to roughly 9 million eukaryotic species. The formation and maintenance
of this diversity requires the accumulation of barriers to reproduction. One of the
most common post-zygotic barriers in plants is hybrid seed inviability (HSI). Despite
its commonality, we know relatively little about the genetic mechanisms and evolutionary
forces which are responsible for this barrier, particularly in naturally co-occurring
species. Here I tested the role of parental conflict in HSI between co-occurring monkeyflowers
in the M. guttatus species complex. I assessed the strength and directionality of
HSI within and between phenotypically described perennial variants of the M. guttatus
species complex. I find substantial HSI between two morphologically described variants,
M. guttatus and M. decorus, amounting to ~30-50% reproductive isolation. Genetically
distinct clades of M. decorus vary in their ability to cross with M. guttatus in both
magnitude and direction of RI. Intriguingly, northern and southern clades of M. decorus
are also incompatible with one another, showing strong, symmetric hybrid seed inviability.
In all cases, HSI is accompanied by parent of origin effects on F1 seed size, consistent
with a role of resource allocation to hybrid inviability. Parent of origin effects
on reciprocal F1s were not limited to final size. I characterize the developmental
trajectory of seeds between M. guttatus and both the northern and southern clades
of M. decorus. Hybrid seeds show similar developmental trajectories depending on their
end fate (i.e. viable vs inviable), despite differing in the maternal and paternal
contributors in these crosses. Inviable seeds are characterized by patterns of paternal
excess; chaotic and malformed endosperm. Viable hybrid seeds are characterized by
maternal excess; limited, and precocious endosperm development. Relatively normal
embryo development early on suggests that hybrid seed inviability stems, in part,
from malformed endosperm. Lastly, I use a combination of modeling, next generation
sequencing, and genotyping approaches to determine the genetic architecture and basis
of HSI. I find that the genetic basis of HSI is complex, wherein several maternally
and paternally inherited nuclear loci interact to cause HSI. In total, I show the
presence of multiple perennial species in the M. guttatus species complex. These species
show little phenotypic or obvious ecological differentiation, but are genetically
unique and have substantial post-zygotic reproductive isolation, namely through the
formation of inviable seeds. Patterns of seed development and final size are indicative
of parent of origin effects on resource allocation to endosperm. Despite relatively
low genetic differentiation for the group, the genetic basis of HSI is quite complex,
involving multiple maternally and paternally interacting alleles. Future work will
be needed to determine the identities of these genes, as well as patterns of repeatability
across the complex.</p>
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