Magister Artium - MA / This thesis analyses post-independence Namibian Heritage and identity discourse and its contestations through the contemporary public performance of olufuko. Olufuko is the ritual of female initiation that marks the transition of young girls into adulthood. The initiation has been an important aspect of the Aawambo women's identity that live in north-central Namibia and southern Angola as it is believed to legitimise womanhood. I show how Owambo residents embrace regional or ethnic diversity through the performance of olufuko as a way of expressing their belonging. Throughout the thesis, I also reflect on the fact that through national attendance at, participation in, and performing of olufuko by state representatives and individuals, from all the regions of Namibia and beyond, people have expressed their belonging to a nation state. During olufuko ceremonies, both regional and national state representatives advocated the ideas of nation-building through 'unity in diversity', which emphasises the diversity of ethnic backgrounds while harmoniously coexisting. Following Becker (2004), and Becker and Lentz (2013), my central argument is that in the contemporary dispensation, national citizenship in Namibia appears to be defined largely through the emphasis on regional or ethnic diversity. In my discussion, I show how the state appropriated and mediated the olufuko ceremony as a national event, though it was performed at the regional level. I show how national identity was visibly represented by national symbols such as the national flag and anthem and how it was audibly live broadcasted by state television and radio during the event. This signified the event as national. The thesis further investigates how national heritage is discussed in post-colonial Namibia by looking into the controversies between the state and ELCIN religious leaders which emanated from the performance of olufuko. The thesis is based on ethnographic research, which was conducted between December 2012, during olufuko ceremonies that took place in villages in Ombadja, and August 2013, when it culminated in participant observation during the public olufuko ceremony at Outapi, Ombalantu.

No description available.

The ability to sense and respond to environmental cues is crucial for the survival of all organisms. This response is often manifested by exerting control at different levels of gene expression, i.e. transcription, translation and post translation levels. Global control of protein synthesis is frequently exercised at the initial step of translation initiation and is generally achieved by changes in the phosphorylation state of initiation factors or the regulators that interact with them. The formation of ternary complex (TC) is considered first step of translation initiation and depends on the recycling of inactive eIF2-GDP to active eIF2-GTP form. This nucleotide exchange reaction is catalyzed by the eukaryotic initiation factor-2B (eIF2B). eIF2B is composed of a regulatory sub-complex of alphaβdelta subunits and a catalytic sub-complex of the γε subunits. The guanine nucleotide exchange activity of eIF2B is regulated by phosphorylation of eIF2alpha and additionally in mammalian cells, by direct phosphorylation of eIF2B at multiple sites in ε subunit, where most of the catalytic activity of eIF2B resides. Recent unpublished studies in the Pavitt laboratory identified novel phosphorylation sites by Mass Spectrometry in γ and ε subunits of eIF2B catalytic sub-complex. In order to study the functional significance of these phospho-sites for translation initiation, Site Directed Mutagenesis (SDM) was performed to generate Ser to Ala mutants. All mutations are viable and have no significant growth defect on rich or minimal media; however the significance of these sites in yeast growth became apparent by growing yeast in different stress conditions (e.g. Rapamycin, Torin1, amino acid starvation and 1-butanol). Effects on the phosphorylation pattern at these sites were monitored by using custom generated phospho-specific antibodies. All phosphorylation events appear independent of the eIF2alpha kinase (Gcn2p in yeast). The phosphorylation of ε-S528 depends on the presence of ε-S525. This study finds that addition of rapamycin, Torin1, amino acid starvation and butanol, which each inhibits global translation initiation, alters the phosphorylation pattern at ε-S435, ε-S525 and ε-S528 sites. Linking growth to phosphorylation, it appears that phosphorylation at ε-S435 and ε-S525 is directly proportional to growth. Phosphorylation of ε-S435 is necessary for effect of eIF2alpha-Ser51 phosphorylation on protein synthesis while phosphorylation of ε-S528 seems to be a target of various mechanisms. This study also suggests that eIF2Bε may be a key player of the cell cycle progression and phosphorylation changes can serve as marker for the regulation of eIF2B activity. The kinases responsible for phosphorylation at these sites are not yet known in yeast. Further investigation is required to find the functional significance of alterations in phosphorylation pattern to definitively establish eIF2Bε phosphorylation as a mechanism for regulating eIF2B activity in yeast. Models are presented to account for the results obtained that show how phosphorylation of eIF2Bε at these sites may contribute to the control of protein synthesis.

Meiosis is the unique process in which diploid cells undergo two consecutive divisions to produce haploid daughter cells. It is indispensable for sexual reproduction in all eukaryotic organisms and maintains proper chromosome number through generations. An integral step in the meiotic program is genetic recombination; recombination is required for a successful reductional division. In the yeast Saccharomyces cerevisiae, recombination is initiated by DNA double strand breaks (DSBs) that are created by ten recombination initiation proteins. Similar phenotypes are observed when any of these genes is mutated. This has made the mechanism by which these proteins function to initiate recombination difficult to unravel. One hypothesis is that these proteins form a functional complex for activity, in which all (or most) of them physically interact. The work described in Chapter 2 contributes to understanding the putative DSB-producing recombination initiation complex, suggesting there is substantial flexibility among initiation protein interactions. The results are also consistent with the view that the proteins assemble on the DNA. Studies in Chapter 3 examined the recombination initiation protein interactions during DSB formation in more detail using a novel experimental approach. While the initial experiments using this approach produced unexpected results, the assay is a promising tool for the future. In addition to creating DSBs, a subset of the initiation proteins perform a second function during early meiosis; they create a recombination initiation signal (RIS) to delay the onset of the reductional division in wild-type cells. Although the signal and the downstream target are well-defined, less is known about how the RIS is transduced to the downstream target. The work in Chapter 4 contributes to defining this transduction, and therefore enhances our understanding of the relationship between the recombination initiation proteins and the reductional division.

Doctor of Philosophy / Binocular rivalry refers to the perceptual alternation that occurs while viewing incompatible images, in which one monocular image is dominant and the other is suppressed. Rivalry has been closely studied but the neural site at which it is initiated is still controversial. The central claim of this thesis is that primary visual cortex is responsible for its initiation. This claim is supported by evidence from four experimental studies. The first study (described in Chapter 4) introduces the methodology for measuring visual sensitivity during dominance and suppression and compares several methods to see which yields the greatest difference between these two sensitivities. Suppression depth was measured by comparing the discrimination thresholds to a brief test stimulus delivered during dominance and suppression phases. The deepest suppression was achieved after a learning period, with the test stimulus presented for 100 ms and with post-test masking. The second study (Chapter 5) compares two hypotheses for the mechanism of binocular rivalry. Under eye suppression, visibility decreases when the tested eye is being suppressed, regardless of the test stimulus’s features. Feature suppression, however, predicts that reduction of visibility is caused by suppression of a stimulus feature, no matter which eye is suppressed. Eye suppression claims that monocular channels in the visual system alternate between dominance and suppression, while Feature suppression assumes that the features of stimuli inhibit each other perceptually in the high-level cortex. The experiment used a test stimulus similar in features to one, but not the other, rivalry-inducing stimulus. Test sensitivity was found to be lowered when the test stimulus was presented to the eye whose rivalry-inducing stimulus was suppressed. Sensitivity was not lowered when the test stimulus was presented to the other eye, even when the test shared features with the suppressed stimulus. The conclusion is that feature suppression is weak or does not exist without eye suppression, and that rivalry therefore originates in the primary visual cortex. If binocular rivalry is initiated in the primary visual cortex, stimuli producing no coherent activity in that area should produce no rivalry. In the third study (Chapter 6) this idea was tested with rotating arrays of short-lifetime dots. The dots with the shortest lifetime produced an image with no rotation signal, and an infinite lifetime produced rigid rotation. Subjects could discriminate the rotation direction with high accuracy at all but the shortest lifetime. When the two eyes were presented with opposite directions of rotation, there was binocular rivalry only at the longest lifetimes. Stimuli with short lifetimes produce a coherent motion signal, since their direction can be discriminated, but do not produce rivalry. A simple interpretation of this observation is that binocular rivalry is initiated at a level in the visual hierarchy below that which supports the motion signal. The model supported by the results of previous chapters requires that binocular rivalry suppression be small in the primary visual cortex, and builds up as signals progress along the visual pathway. This model predicts that for judgements dependent on activity in high visual cortex: 1. Binocular rivalry suppression should be deep; 2. Responses should be contrast invariant. The fourth and last study (chapter 7) confirmed these predictions by measuring suppression depth in two ways. First, two similar forms were briefly presented to one eye: the difference in shapes required for their discrimination was substantially greater during suppression than during dominance. Second, the two forms were made sufficiently different in shape to allow easy discrimination at high contrast, and the contrast of these forms was lowered to find the discrimination threshold. The results in the second experiment showed that contrast sensitivity did not differ between the suppression and dominance states. This invariance in contrast sensitivity is interpreted in terms of steep contrast-response functions in cortex beyond the primary visual area. The work in this thesis supports the idea that binocular rivalry is a process distributed along the visual pathway. More importantly, the results provide several lines of evidence that binocular rivalry is initiated in primary visual cortex.

A mesoscale tropical channel model is constructed to study the long-standing problem of the initiation of the Madden-Julian Oscillation (MJO). Two observed cases of MJO are chosen, one in boreal spring and one in boreal winter, without a priori knowledge of their initiation mechanism. With initial and lateral boundary conditions provided by a global reanalysis, this model is able to reproduce the initiation and gross features of two observed MJO events up to two months after the start of simulations. This leads to a conjecture that these two MJO events are generated by the influences from the lateral boundaries. This conjecture is supported by a series of sensitivity tests. These sensitivity tests demonstrate that the simulated MJO initiation does not critically depend on detailed characteristics of sea surface temperature (varying vs. constant in time, mean distribution from boreal spring vs. winter), initial conditions (within a 10 day period, perturbations in the initial conditions), the latitudinal location of the lateral boundaries (21 - 45˚N and S), and even latent heating and moist processes. The only factor found critical to the reproduction of the MJO initiation is time varying lateral boundary conditions from the reanalysis. When such lateral boundary conditions are replaced by time independent conditions, the model fails to reproduce the MJO initiation. The analysis of moist static energy has revealed that the discharge-recharge mechanism is not sufficient for the MJO initiation in the model. It is found that the latitudinal transport of westerly momentum from the extratropics is crucial in generating the lower tropospheric westerlies in the reanalysis and model. The energy source for the extratropical perturbation is through extraction of kinetic energy from the mean flow. The estimation of wave activity flux has revealed that there is a major region over the southern Indian Ocean, which produces wave activity flux towards the tropical genesis region of the MJO initiation. We have also investigated the time-scale of the boundary conditions that are responsible for the MJO initiation. Additions of small perturbations in the boundary conditions, and use of 10-day interpolated boundary conditions do not affect the MJO initiation. Thus boundary conditions responsible for the MJO initiation in the model must have time scales greater than 10 days, indicating that the shorter time scale stochastic forcing through the lateral boundaries did not play any major role. The estimation of the zonal momentum budget for the MJO initiation region has revealed the importance of the advective terms, particularly by the meridional winds before the onset of the MJO. The importance of the extratropical influences in initiating the MJO in the channel model leads to a speculation that a multi-year simulation using a tropical channel model would also produce reasonable MJO statistics if forced by time varying boundary conditions. Interestingly, the MJO statistics in the multi-year simulation using a tropical channel model is found to be not better than the global models. Increase of horizontal resolution and use of a different cumulus scheme did not improve the MJO simulation. We found that the error in the mean state was the main reason for the lack of MJO statistics in the model. The model took less than five days for the error to reach its climate bias. Thus, a good simulation of the mean state is important for the successful simulation of the MJO. Implications of these results are discussed. In short, this study has shown that the extratropical influences can be an efficient mechanism for the MJO initiation and calls for further research attention to this mechanism that has been somewhat neglected by mainstream MJO research.

Thesis (M.A.)--Memorial University of Newfoundland, 2002. / Bibliography: leaves 185-199.

The S1 genome segment of avian reovirus is functionally tricistronic, encoding three independent protein products (named p10, p17 and ?C) from three sequential, partially overlapping open reading frames (ORFs). The dogma of translation initiation, the cap-dependent scanning model, suggests that ribosomes would normally only translate the 5?-proximal ORF. Four alternate mechanisms of translation initiation could account for translation of the downstream ?C ORF; an IRES element, reinitiation, ribosome shunting, and leaky scanning. The objective of my doctoral research was to investigate the translation initiation mechanisms that are operative on the S1 mRNA. Translation of the p10 and p17 ORFs was revealed to be coordinated via standard leaky scanning, while none of the known mechanisms of translation initiation could account for expression of the ?C ORF. Further investigation determined that two alternate cap-dependent mechanisms contribute to translation initiation at the ?C AUG codon. The first mechanism involves a modified version of enhanced leaky scanning. Although insertion of upstream elements known to impede scanning ribosomal subunits dramatically inhibited translation of the downstream ORF in the context of other mRNAs, the same elements only marginally reduced ?C translation. Specific features of the S1 mRNA therefore function to promote leaky scanning and translation of the ?C ORF. The inability to eliminate ?C expression beyond a threshold retention level of ~20-30%, despite the presence of eight upstream start codons that should eliminate leaky scanning, strongly suggests that ribosomes must also utilize a scanning-independent means to access the internal ?C start site. This mechanism for ?C translation initiation, which I termed ribosome handoff, allows ribosomes to bypass upstream elements, and requires a sequence-dependent translation enhancer element present within S1 nucleotides 366-392 that may function to mediate handoff via complementarity with 18S ribosomal RNA. Translation initiation at the ?C start site is therefore made possible by two alternative mechanisms, enhanced leaky scanning and ribosome handoff from the 5?-cap. The novelty of these two mechanisms highlights the complexity of the translation initiation process and the potential heterogeneity of cellular ribosomes, which raises the possibility that internal initiation may be far more common than currently appreciated.

Mémoire numérisé par la Division de la gestion de documents et des archives de l'Université de Montréal

Doctor of Philosophy / Binocular rivalry refers to the perceptual alternation that occurs while viewing incompatible images, in which one monocular image is dominant and the other is suppressed. Rivalry has been closely studied but the neural site at which it is initiated is still controversial. The central claim of this thesis is that primary visual cortex is responsible for its initiation. This claim is supported by evidence from four experimental studies. The first study (described in Chapter 4) introduces the methodology for measuring visual sensitivity during dominance and suppression and compares several methods to see which yields the greatest difference between these two sensitivities. Suppression depth was measured by comparing the discrimination thresholds to a brief test stimulus delivered during dominance and suppression phases. The deepest suppression was achieved after a learning period, with the test stimulus presented for 100 ms and with post-test masking. The second study (Chapter 5) compares two hypotheses for the mechanism of binocular rivalry. Under eye suppression, visibility decreases when the tested eye is being suppressed, regardless of the test stimulus’s features. Feature suppression, however, predicts that reduction of visibility is caused by suppression of a stimulus feature, no matter which eye is suppressed. Eye suppression claims that monocular channels in the visual system alternate between dominance and suppression, while Feature suppression assumes that the features of stimuli inhibit each other perceptually in the high-level cortex. The experiment used a test stimulus similar in features to one, but not the other, rivalry-inducing stimulus. Test sensitivity was found to be lowered when the test stimulus was presented to the eye whose rivalry-inducing stimulus was suppressed. Sensitivity was not lowered when the test stimulus was presented to the other eye, even when the test shared features with the suppressed stimulus. The conclusion is that feature suppression is weak or does not exist without eye suppression, and that rivalry therefore originates in the primary visual cortex. If binocular rivalry is initiated in the primary visual cortex, stimuli producing no coherent activity in that area should produce no rivalry. In the third study (Chapter 6) this idea was tested with rotating arrays of short-lifetime dots. The dots with the shortest lifetime produced an image with no rotation signal, and an infinite lifetime produced rigid rotation. Subjects could discriminate the rotation direction with high accuracy at all but the shortest lifetime. When the two eyes were presented with opposite directions of rotation, there was binocular rivalry only at the longest lifetimes. Stimuli with short lifetimes produce a coherent motion signal, since their direction can be discriminated, but do not produce rivalry. A simple interpretation of this observation is that binocular rivalry is initiated at a level in the visual hierarchy below that which supports the motion signal. The model supported by the results of previous chapters requires that binocular rivalry suppression be small in the primary visual cortex, and builds up as signals progress along the visual pathway. This model predicts that for judgements dependent on activity in high visual cortex: 1. Binocular rivalry suppression should be deep; 2. Responses should be contrast invariant. The fourth and last study (chapter 7) confirmed these predictions by measuring suppression depth in two ways. First, two similar forms were briefly presented to one eye: the difference in shapes required for their discrimination was substantially greater during suppression than during dominance. Second, the two forms were made sufficiently different in shape to allow easy discrimination at high contrast, and the contrast of these forms was lowered to find the discrimination threshold. The results in the second experiment showed that contrast sensitivity did not differ between the suppression and dominance states. This invariance in contrast sensitivity is interpreted in terms of steep contrast-response functions in cortex beyond the primary visual area. The work in this thesis supports the idea that binocular rivalry is a process distributed along the visual pathway. More importantly, the results provide several lines of evidence that binocular rivalry is initiated in primary visual cortex.