In this study, predictable electrosensory input was experimentally
created by repetitive pairings of a peripheral excitatory electrosensory stimulus with either ventilatory motor commands or passive fin movements, both of which are known to be represented among the internal reference signals of the molecular layer. In both cases, the development of a cancellation signal that suppresses predictable electrosensory input was apparent in AEN responses: the response to the electrosensory stimulus declined during repeated pairings, and removal of the electrosensory stimulus revealed suppressed activity time-locked to the period of the suddenly absent electrosensory stimulus. Using this coupling paradigm, the functional properties of multiple cancellation signals within a single AEN were examined. First, multiple cancellation signals associated with distinct internal reference signals in the molecular layer are shown to exist within a single AEN and are modified independently, suggesting that separate cancellation signals for distinct behaviors may also exist, and can be stored and modified without affecting one another. Second, overlapping cancellation signals associated with distinct internal reference signals are additive in a subset of AENs, although not all AENs had combined cancellation signals that were significant or stronger than singular cancellation signals. These results support the idea that a single behavior may have several component cancellation signals that are associated with different aspects of the behavior. Together, the component cancellation signals may work in conjunction to more
effectively suppress reafference associated with that behavior. We propose that a functional role for multiple cancellation signals, shown in this study to be independent and additive, may be to provide sensory predictions that suppress dynamic, complex patterns of reafference that result from continuously, intermittently or concurrently performed behaviors.

In this thesis, I aimed to characterize the early prophase events that facilitate homolog pairing and pairing reinforcement. I investigated two nonhomologous pairing processes that occur in yeast for their potential role in homolog pairing. One of these processes, bouquet formation, is defined by a clustering of chromosomes,
tethered by their telomeres, to a subregion of the nuclear envelope. The other, centromere coupling, is characterized by rapid, homology-independent associations between chromosomes at their centromeres. I created a strain in which both of these processes were abolished and observed the effect on homolog pairing. In this strain,
homolog pairing is still achieved, albeit at a delayed rate compared to a wild-type strain. We conclude that these processes are not required for homolog pairing, but may aid in the efficiency of homology recognition.

I also aimed to characterize the steady-state dynamics of the SC. The SC, composed in budding yeast of the transverse filament protein Zip1 and other proteins, assembles along the length of paired homologs in a recombination-dependent manner and is maintained at its full-length state until late meiosis I. Previous observations in
our lab demonstrated that this structure has some dynamic character, with subunits continually incorporated into the full-length, steady-state structure. I constructed strains bearing fluorescent Zip1 and/or an inducible wild-type Zip1 expression system to determine whether subunits are removed from this structure at the steady state. My
observations indicate that subunits are not significantly removed from the steady-state
SC, and that furthermore, this structure appears to increase in Zip1 content throughout the duration of the steady state with no apparent size constraint. Preliminary data also suggests that subunit removal does not occur locally at sites of crossover
recombination. Furthermore, the rate of SC assembly appears to be dependent on Zip1 concentration, with nuclei overexpressing ZIP1 constructing full-length SCs more rapidly.

Throughout my thesis work, I also worked to characterize a collection of Zip1 alleles mutated at residues that may be sites of Zip1 phosphorylation. I identified mutants with meiotic phenotypes, indicating that these mutants may be interesting for further characterization.

It is shown that in the majority of cases, the reaction proceeds to the benzhydryl alkyl ether corresponding to the nucleophile used. The primary mechanism by which this reaction occurs is shown via electrolyses and computational modeling to proceed via a cation radical delocalized across the carbonyl oxygen and one phenyl ring of the benzhydryl moiety in a novel type of conjugation specific to α-benzhydryl ketones. This mechanism stands in contrast to that of anodic oxidation of 2,2-diphenylacetaldehyde, which was shown previously to be oxidized primarily via its enol.

Our results show that, in these river meanders, bedform formation, morphology and stability are driven by stream power. Low Froude numbers (0.05-0.10) indicate that the river is usually in a state of equilibrium, but that it is punctuated by short intervals of bedform destruction during high discharge. Mean and median grain size were similar throughout the meanders and all parts of the bedforms suggesting the importance of hydraulic sorting.

Field data included imaging the river using sidescan sonar, collecting sediment samples, measuring river discharge using an acoustic Doppler current profiler, and using USGS gage heights at Hartford and Middletown. Modeling was done with CCHE2D, a two-dimensional flow and sediment transport model developed at the National Center for Computational Hydroscience and Engineering.

The grain size analysis shows that the first glacial evidence occurred during the Lower Oligocene in the Eastern Weddell Sea and that the West Antarctic Ice Sheet had been fully formed by the Middle Miocene. The 40Ar/39Ar ages of detrital hornblendes and U-Pb ages of detrital zircons show shifting source areas for the Weddell Sea icebergs from the Middle Miocene to the Early Pliocene. These analyses lead to the conclusion that most of the ice rafted debris is sourced from East Antarctica, even after the formation of the West Antarctic Ice Sheet. There is also evidence for a destabilization event, similar to an event observed by previous studies (Williams et al., 2010), during the Late Miocene and Early Pliocene. Age provenance indicates that distant icebergs arrived and that there was a shift in the method of coarse material deposition from ice rafting to turbidites.

The function of histone H1 is poorly understood. Early in vitro studies
suggested that histone H1 facilitated chromatin condensation. As a result of its role in DNA packaging, it was thought that histone H1 might serve as a transcriptional repressor. However, initial in vivo studies in Saccharomyces cerevisiae have shown that Hho1 (histone H one) was not essential for cell viability, and its deletion yielded no detectable changes in chromatin structure, growth rates, or transcriptional silencing at the constitutively silenced loci.

In order to clarify the role of Hho1 and its mechanism of function, my
research project aims to explore the interaction between Hho1 and the histone
octamer proteins H3 and H4. The characterization of this relationship will help us determine the nature of Hho1’s influence on transcriptional silencing.

To examine the Hho1 and nucleosome interaction, we eliminated the HHO1
gene in strains containing particular histone H3 or histone H4 mutations and looked for the suppression or exacerbation of silencing phenotypes at the three constitutively silenced loci in Saccharomyces cerevisiae: the HM loci, the telomeres, and the rDNA repeats. We selected nucleosomal mutants that were most likely to impact transcriptional silencing or interact with Hho1. These regions of these mutations included histone tails, the DNA entrance and exit site, the LRS (loss of rDNA silencing) region, and modifiable residues.

We observe significant changes in transcriptional silencing in nucleosomal
mutants upon the deletion of HHO1, indicating a functional interaction between Hho1 and the nucleosome. This interaction is complicated, as the deletion of HHO1 may decrease or increase transcriptional silencing depending on the mutant allele. Interestingly, the influences of Hho1 on transcriptional silencing at the telomere and rDNA do not correlate. We took advantage of these differences to identify mutants that significantly contribute to global or locus-specific changes in silencing. Strikingly, using a Monte Carlo method bootstrapping without replacement approach, we determined that histone H3 tail mutants significantly contribute to a decrease in silencing and that lysine mutants significantly contribute to an increase in silencing at both the telomere and rDNA upon the deletion of HHO1. This suggests that these mutants impact a global Hho1-dependent transcriptional silencing effect. In addition, histone H4 mutants are significantly overrepresented in strains that exhibit a decrease in telomeric and an increase in rDNA silencing upon the deletion of HHO1. These mutants, therefore, impact a locus-specific Hho1-dependent transcriptional silencing effect. Our observations lead to hypotheses about the role of Hho1 that provide a basis for future experimentation.