The goal of the Thesis is to analyze the issue that is related to the extinction of the rights and obligations of business relations. Trading obligations are very specific group of legal relations. Without them it is imposible to imagine a faultless performance and successful business. The author in this thesis attempts to address all relevant aspects of the topic. To achieve the above objectives, the author intends to use a particular method of interpretation of legal norms. This method will be complemented by an authentic interpretation of legal norms, doctrinal interpretation, legal interpretation or the relevant case law. Analysis of these areas can conclude that there is a large area in terms of legislation and legal theory, systematic non-uniform. One of the main complexities of contract law, the author sees in the dualism legislation. From the available case law of the Supreme Court or Superior Courts may conclude that in most practical application of legal problems arose on the fulfillment of commitments and cancellation. These are the most frequent reasons for termination of the legal obligations. Another finding is the inconsistency of terminology and the Civil Commercial Code.

La transcription de l’ADN en ARN constitue la première étape de l’expression d’un gène. Durant les dix dernières années, plusieurs études ont montré qu’environ 80-90% du génome est transcrit et que la transcription peut démarrer presque partout. Ce phénomène, connu sous le nom de transcription envahissante, représente une menace sérieuse contre l’expression correcte du génome car il peut interférer non seulement avec d’autres évènements de transcription mais également avec n’importe quel procédé impliquant l’ADN. Une terminaison sélective est donc un mécanisme de la plus haute importance pour la stabilité du génome et la correcte régulation de l’expression des gènes. Ici nous décrivons la terminaison road-block, un nouveau mécanisme de la terminaison par l’ARN polymerase II, qui a pour fonction de limiter la transcription envahissante et de limiter les conséquences d’une translecture au niveau des sites de terminaison canoniques de S.cerevisiae. Nous démontrons également que plusieurs facteurs de transcription peuvent entrainer cette terminaison et que certains sites génomiques y sont associés. De plus, nous explorons également la possibilité que ces terminaisons road-block puissent contribuer à rendre spécifiques les origines de réplication. / Transcription of DNA into RNA intermediates constitutes the first step in gene expression. During the last decade, several studies showed that about 80-90% of the genome is transcribed, and that transcription can initiate almost anywhere. This process—known as pervasive transcription—represents a serious threat to proper gene expression as it has the potential to interfere with not only other transcription events, but any DNA-based process. Selective transcription termination is therefore a mechanism of paramount importance for genome transcriptome stability and correct regulation of gene expression. Here we describe road-block termination, a novel termination mechanism for RNA polymerase II that functions to limit pervasive transcription and buffer the consequences of readthrough transcription at canonical terminators in S.cerevisiae. We show that several transcription factors can elicit this termination and that a number of unexpected genomic loci are associated with it. Additionally, we explore the possibility that road-block termination might contribute to specification of replication origins.

La transcription cachée est un phénomène répandu aussi bien chez les eucaryotes que chez les procaryotes. Elle se caractérise par une production massive d’ARNs non-codants au niveau de régions non-annotées du génome et est potentiellement dangereuse pour la cellule car elle peut interférer avec l’expression normale des gènes. Chez S. cerevisiae, l’hélicase Sen1 induit la terminaison précoce de la transcription non-codante et joue ainsi un rôle clé dans le contrôle de la transcription cachée. Sen1 est très conservée et des mutations dans son homologue humain, senataxin (SETX), ont été associées à des maladies neurodégénératives. Malgré de nombreuses recherches menées sur ces protéines, leurs propriétés biochimiques ainsi que leurs mécanismes d’action restent peu connus. Durant ma thèse, j’ai étudié le mécanisme de terminaison par Sen1.Premièrement, j’ai caractérisé les activités biochimiques de Sen1 et analysé comment elles permettent d’induire la terminaison. Pour cela, j’ai utilisé un ensemble de techniques in vitro, notamment un système de transcription-terminaison qui contient uniquement des composants purifiés : Sen1, l’ARN polymérase II (Pol II) et les ADN matrices. Ce système permet de modifier les différents éléments de façon contrôlée afin de comprendre leur rôle précis dans la terminaison. J’ai tout d’abord analysé la fonction des différents domaines de Sen1 dans la terminaison. Sen1 est une protéine de taille importante qui possède un domaine central catalytique flanqué par deux domaines impliqués dans l’interaction avec d’autres facteurs. J’ai montré que le domaine hélicase est suffisant pour déclencher la terminaison de la transcription in vitro. Ensuite, j’ai montré que Sen1 utilise l’énergie de l’hydrolyse de l’ATP pour se déplacer sur des acides nucléiques simple bras (ARN et ADN) dans le sens 5’ vers 3’. J’ai alors étudié le rôle des différents acides nucléiques du système dans la terminaison par Sen1 et j’ai montré que l’interaction de Sen1 avec l’ADN n’est pas nécessaire; en revanche Sen1 doit s’associer à l’ARN naissant et se déplacer vers la polymérase. J’ai aussi montré qu’une fois que Sen1 entre en collision avec la Pol II, elle y exerce une action mécanique qui conduit à la terminaison uniquement quand la Pol II marque une pause. Cela indique que la terminaison est fortement dépendante de la pause transcriptionnelle. Deuxièmement, en collaboration avec le groupe d’E. Conti, nous avons réalisé une analyse structure-fonction du domaine hélicase de Sen1. Nous avons observé que Sen1 présente une organisation similaire à celle d’autres hélicases proches avec un core composé de deux domaines de type RecA avec plusieurs domaines auxiliaires. En général, le core est très conservé au sein des hélicases proches, alors que les domaines accessoires ont des caractéristiques distinctes qui confèrent des propriétés spécifiques aux différentes hélicases. En effet, nous avons identifié un sous-domaine spécifique à Sen1 mais conservé au cours de l’évolution que nous avons appelé le “brace”. Nous avons également détecté des différences notables au niveau d’un autre domaine accessoire que nous avons nommé le “prong”. Nous avons pu montrer que le “prong” est essentiel pour la terminaison par Sen1. Nos données suggèrent que les caractéristiques structurales spécifiques de Sen1 que nous avons révélées sont des déterminants majeurs de son activité dans la terminaison de la transcription. Finalement, nous avons utilisé Sen1 comme modèle pour étudier des mutations dans SETX qui sont associées à des maladies neurodégénératives. Nous avons introduit chez Sen1 une partie des mutations liées à des maladies et nous avons réalisé une caractérisation biochimique complète de chaque mutant. Nous avons ainsi montré que toutes les mutations sont fortement délétères pour la terminaison de la transcription. En conclusion, nos résultats ont permis d’améliorer la compréhension de l’origine des maladies provoquées par des mutations dans SETX. / Pervasive transcription is a common phenomenon both in eukaryotes and prokaryotes that consists in the massive production of non-coding RNAs from non-annotated regions of the genome. Pervasive transcription poses a risk that needs to be controlled since it can interfere with normal transcription of canonical genes. In S.cerevisiae, the helicase Sen1 plays a key role in restricting pervasive transcription by eliciting early termination of non-coding transcription. Sen1 is highly conserved across species and mutations in the human Sen1 orthologue, senataxin (SETX), are associated with two neurological disorders. Despite the major biological relevance of Sen1 proteins, little is known about their biochemical properties and precise mechanisms of action. During my PhD I have studied in detail the mechanisms of termination by Sen1.In a first project, I have characterized the biochemical activities of Sen1 and investigated how these activities partake in termination. To this end I have employed a variety of in vitro approaches, including a minimal transcription-termination system containing only purified Sen1, RNA polymerase II (RNAPII) and DNA transcription templates that allows modifying the different elements of the system in a controlled manner to understand their role in termination. First, we have analysed the function of the different domains of Sen1 in termination. Sen1 is a large protein composed of a central catalytic domain flanked by additional domains with proposed roles in protein-protein interactions. We have demonstrated that the central helicase domain is sufficient to elicit transcription termination in vitro. Next, we have shown that Sen1 can translocate along single-stranded nucleic acids (both RNA and DNA) from 5’ to 3’. Then, we have analysed the role of the different nucleic acid components of the elongation complex (i.e. nascent RNA and DNA transcription templates) in termination. Our results indicate that termination does not involve the interaction of Sen1 with the DNA but requires Sen1 translocation on the nascent RNA towards the RNAPII. Importantly, we show that upon encountering RNAPII, Sen1 can apply a mechanical force on the polymerase that results in transcription termination when RNAPII is paused under certain conditions. This indicates that RNAPII pausing is a strict requirement for Sen1-mediated termination. In a second project, in collaboration with the group of E. Conti we have performed a structure-function analysis of the helicase domain of Sen1. Comparison of Sen1 structure with that of other related helicases has revealed an overall similar organization consisting in two tandem RecA-like domains from which additional accessory subdomains protrude. In general, the core RecA-like domains are very well conserved among related helicases and most variation is found in the accessory subdomains, that often confer specific characteristics to different helicases. Indeed, we have found that Sen1 contains a unique but evolutionary conserved structural feature that we have dubbed the “brace”. In addition, Sen1 is different from other helicases in an auxiliary subdomain that we have named the “prong”. Importantly, we have shown that the integrity of this subdomain is critical transcription termination by Sen1. We propose that the specific features identified in our structural analyses are important determinants of the transcription termination activity of Sen1. Finally, we have used Sen1 as a model to investigate the molecular effect of SETX mutations linked to neurodegenerative diseases. We have introduced disease-associated mutations in Sen1 and performed a complete biochemical characterization of the different mutants in vitro. Importantly, we found that all mutants were severely affected in transcription termination. Taken together, our results elucidate the key structural determinants of the function of Sen1 and shed light on the molecular origin of the diseases associated with SETX mutations.

This dissertation examines how different forms of state capacity affect the decision of terror groups to end their campaign. Building a theoretical framework about the relationship between state capacity and terrorist group termination, I address the following research questions: How do terror groups respond to the changes in non-repressive forms of state's capacity, such as bureaucratic capacity, extractive capacity, and how do those responses of terror groups affect the chance of their demise? How do the changes in non-repressive forms of state capacity affect the likelihood of termination of particular types of terror groups, specifically ethnic terror groups? And finally, how do security forces representing repressive capacity of states affect the probability of a terrorist group end? I argue that as the state fighting the terror group increases its capacity, that will generate an incentive for the terror group to respond to increasing state capacity to secure its survival and maintain its existence. As the terror group produces responses to increasing state capacity in terms of rebuilding its capacity to operate and keeping its popular support base intact, it will be less likely to end its terror campaign. This argument is particularly relevant for terror groups operating on behalf of a certain ethnic or religious group. I test this theory by doing a cross-national quantitative analysis as well as doing a qualitative analysis on the PKK's terror campaign in Turkey in the period of 1984-2013. I find that increasing extractive capacity and bureaucratic capacity of states encourages terror groups to engage in coercive and non-coercive actions to survive increasing state capacity, thereby reducing the chances of ending its terror campaign. I also argue that security forces, who represent repressive capacity of states, also play a role on the decision of terror groups to end their campaigns. By focusing exclusively on militarized law enforcement forces, I contend that the presence of these forces might either enhance the chances of survival of terror groups or increases the risk of the demise of these groups. Whether having these forces increases or decreases the likelihood of terror group end is a function of the capacity of the state to control the actions and behaviors of security forces. By constructing a time series cross-sectional data set on militarized law enforcement forces, I test these arguments and find that having militarized law enforcement forces decreases the risk of terror group end, but as the state's bureaucratic capacity increases, having these forces increases the likelihood that the terror group will decide to end its campaign. These empirical findings have several theoretical implications for the extant literature on state capacity and terrorism, and they also have implications for policymakers in terms of designing an effective counter-terrorism policy to deal with the threats from terrorist groups.

In the circular Escherichia coli chromosome, two replisomes are assembled at the unique origin of replication and drive DNA synthesis in opposite directions until they meet in the terminus region across from the origin. Despite the difference in rates of the two replisomes, their arrival at the terminus is synchronized through a highly specialized system consisting of the terminator protein (Tus) bound to the termination sites (Ter). This synchronicity is mediated by the polarity of the Tus−Ter complex that stops replisomes from one direction (non-permissive face) but not the other (permissive face). Two oppositely oriented clusters of five Tus–Ters that each block one of the two replisomes create a “replication fork trap” for the first arriving replisome while waiting for the late arriving one. Despite extensive biochemical and structural studies, the molecular mechanism behind Tus−Ter polar arrest activity remained controversial. Moreover, none of the previous work provided answers for the long-standing discrepancy between the ability of Tus−Ter to permanently stop replisomes in vitro and its low efficiency in vivo. Here, I spearheaded a collaborative project that combined single-molecule DNA replication assays, X-ray crystallography and binding studies to provide a true molecular-level understanding of the underlying mechanism of Tus−Ter polar arrest activity. We showed that efficiency of Tus−Ter is determined by a head-to-head kinetic competition between rate of strand separation by the replisome and rate of rearrangement of Tus−Ter interactions during the melting of the first 6 base pairs of Ter. This rearrangement maintains Tus’s strong grip on the DNA and stops the advancing replisome from breaking into Tus−Ter central interactions, but only transiently. We further showed how this kinetic competition functions within the context of two mechanisms to impose permanent fork stoppage. The rate-dependent fork arrest activity of Tus−Ter explains its low efficiency in vivo and why contradictory in vitro results from previous studies have led to controversial elucidations of the mechanism. It also provides the first example where the intrinsic heterogeneity in rate of individual replisomes could have different biological outcomes in its communication with double-stranded DNA-binding protein barriers.

The master's thesis deals with redundancy payment and other compensations that result from labour relations and service relations. The main task is a description of redundancy payment and notice reasons related to redundancy payment. The thesis describes redundancy payment in the Slovak Republic and compares it with redundancy payment in the Czech Republic. Compensation in the service relationship and officials of territorial self-governing units are discussed. The case law of the Supreme Court is included. The diploma thesis is divided into four chapters. The termination of employment is discussed in the first chapter. The chapter focuses on legal action towards termination of employment. The reasons for termination of employment under the Labour Code related to redundancy payment are described. The second chapter focuses on redundancy payment as the main topic of the thesis. The chapter contains definition and purpose of redundancy payment. The legal redundancy payment and its amount are defined. Further, the calculation of redundancy payment is explained. There is also an explanation of contractual redundancy payment where the parties can agree on redundancy payment. The third chapter describes the termination of employment, redundancy payment under the Slovak Labour Code. It also compares the...

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The tarnished plant bug, Lygus lineolaris (Palisot de Beauvois), is the most important insect pest of cotton, Gossypium hirsutum (L.), in Mississippi. This research project was initiated to gain a better understanding of selected crop production factors that can improve tarnished plant bug integrated pest management. Results suggest that irrigation strategies and varietal pubescence can significantly influence tarnished plant bug management in cotton. Most notably, delaying irrigation for as long as possible and planting hairy varieties can minimize the impact of tarnished plant bug on cotton yields and reduce the number of insecticides needed to manage this pest. Additionally, these results show that tarnished plant bug management is most critical during the first four weeks of flowering. Results from these experiments will be used to improve the current integrated pest management program for tarnished plant bug in cotton and make cotton production more sustainable for Mississippi producers.

Through proper irrigation scheduling and management of damaged cotton, sustainable agricultural withdrawal from the Mississippi River Valley Alluvial Aquifer can be achieved while maximizing net returns. This research was conducted to 1) develop a sensor based irrigation strategy that maximized cotton lint yield and quality, irrigation, and water use efficiency (IWUE) and 2) quantify the effects of timing of damage, intensity, and foliar N on cotton growth and development. Lint yield, fiber quality, and IWUE were optimized using a season-long irrigation threshold of -90 kPa and irrigation terminated 2-weeks before cracked boll. Regardless of cotton variety (early- or late-maturing) or timing of damage, plant height, number of nodes, and lint yield were negatively correlated with the intensity of damage. Moreover, the application of foliar nitrogen to damaged cotton had no effect on plant growth, lint yield, or fiber quality, regardless of N application timing. These data indicate that lint yield, and fiber quality are optimized when cotton varieties are selected based on yield potential, irrigated at -90 kPa threshold, and irrigations are terminated two weeks before cracked boll.