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Biosystematic Studies in Crepidotus and the Crepidotaceae (Basidiomycetes, Agaricales)Aime, Mary Catherine 07 May 2001 (has links)
Fungi of the Crepidotaceae are characterized by saprotrophic habit, filamentous cuticle, and brown-pigmented basidiospores that lack either a germ pore or plage. The majority of species belong to Crepidotus, distinguished by their pleurotoid basidiomata. Because of their diverse morphology, the presence of several conflicting classifications, and lack of data regarding the biology, phenotypic plasticity, or phylogeny of these fungi, the present study sought first to determine phylogenetic relationships among the different taxonomic groups as a basis for addressing other aspects of Crepidotus biology and evolution.
Sequencing analyses show the Crepidotaceae is not monophyletic, and the family concept is revised. Crepidotus and its sister genus Simocybe are found to be monophyletic. At least nine phylogenetic lineages within Crepidotus were uncovered, although relationships between them could not be resolved. However, none of the previously proposed infrageneric classifications are reflective of phylogeny.
Morphological, biological, and phylogenetic species concepts were compared within a single phylogenetic unit, termed the Sphaerula group, showing an unusual amount of phenotypic plasticity exists within species, and a taxonomic revision of these species proposed. Also reported are several unique or unusual aspects of Crepidotus biology, including presence of a prolonged latent period prior to basidiospore germination; spontaneous reversion of differentiated hymenial cells to vegetative growth; and the revelation that structures previously termed pleurocystidia are actually the expression of secondary growth from basidia. Results from mating system, culture, and type studies, reassessment of morphological characters traditionally applied to agaric taxonomy, and a revised life cycle for the Crepidoti are presented. / Ph. D.
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Mitochondrial function in murine skin epithelium is crucial for hair follicle morphogenesis and epithelial-mesenchymal interactionsKloepper, J.E., Baris, O.R., Reuter, K., Kobayash, K., Weiland, D., Vidali, S., Tobin, Desmond J., Niemann, C., Wiesner, R.J., Paus, R. 08 1900 (has links)
No / Here, we studied how epithelial energy metabolism impacts overall skin development by selectively deleting intraepithelial mtDNA in mice by ablating a key maintenance factor (TfamEKO), which induces loss of function of the electron transport chain (ETC). Quantitative (immuno)histomorphometry demonstrated that TfamEKO mice showed significantly reduced hair follicle (HF) density and morphogenesis, fewer intrafollicular keratin15+ epithelial progenitor cells, increased apoptosis, and reduced proliferation. TfamEKO mice also displayed premature entry into (aborted) HF cycling by apoptosis-driven HF regression (catagen). Ultrastructurally, TfamEKO mice exhibited severe HF dystrophy, pigmentary abnormalities, and telogen-like condensed dermal papillae. Epithelial HF progenitor cell differentiation (Plet1, Lrig1 Lef1, and β-catenin), sebaceous gland development (adipophilin, Scd1, and oil red), and key mediators/markers of epithelial–mesenchymal interactions during skin morphogenesis (NCAM, versican, and alkaline phosphatase) were all severely altered in TfamEKO mice. Moreover, the number of mast cells, major histocompatibility complex class II+, or CD11b+ immunocytes in the skin mesenchyme was increased, and essentially no subcutis developed. Therefore, in contrast to their epidermal counterparts, pilosebaceous unit stem cells depend on a functional ETC. Most importantly, our findings point toward a frontier in skin biology: the coupling of HF keratinocyte mitochondrial function with the epithelial–mesenchymal interactions that drive overall development of the skin and its appendages.
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The role of the stubble protease in RhoA signaling during Drosophila imaginal disc morphogenesisMou, Xiaochun 01 January 2004 (has links)
No description available.
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GLI2 Transcriptional Cascade During Mouse Fetal Lung DevelopmentRutter, Martin Edward 01 August 2008 (has links)
The lung is an organ that contains a vast system of airways carefully constructed to achieve maximal surface area in a confined space, requiring guidance from a multitude of developmental factors. The Shh pathway is one such signaling mechanism that is critical to proper lung formation, guiding branching morphogenesis and cellular proliferation through its downstream Gli transcription factors. Additionally, Foxf1 has been shown to be a key developmental factor required for proper lung formation during embryogenesis. Although theorized that the Gli transcription factors are responsible for regulating foxf1 levels, their exact relationship has yet to be revealed. Using five different models for Shh signaling (gli2 null, gli2 over-expressor [hVER-Gli2], gli3 null, Gli3 constitutive repressor [Gli3Δ699] and cyclopamine treated lung explants), I compared and contrasted the role of Gli2 and Gli3 in terms of their effect on cell cycle regulation, and on the expression levels of foxf1 and its potential downstream target genes tbx4, tbx5 and fgf10. I found that ectopic over-expression of gli2 resulted in increased Shh pathway activation, and increased expression of G1/S phase cyclins, which was associated with increased cellular proliferation and lung growth. However, no change in the levels of G1/S phase cyclins due to altered Gli3 signaling was observed. Foxf1 levels positively correlate with the levels of gli2, and appear to be independent of Gli3 activity. The amount of tbx4, tbx5, and fgf10 transcripts were observed to follow the levels of gli2 in the different gli2 mouse models, however, there was no significant change in gli3 null or Gli3Δ699 mice. Finally, by analyzing gene expression at different time points during gestation, I found that while gli2 levels affect foxf1 throughout gestation, the relationship to tbx4, tbx5 and fgf10, occurs only during the latter stages of lung development. I conclude, that Gli2 and not Gli3 appears to be the primary transducer of Shh signaling influencing cyclin regulation, leading to changes in embryonic lung growth. Furthermore, that Gli2 and not Gli3 appears to regulate foxf1 expression levels, and that this may extend downstream to influence tbx4, tbx5 and fgf10 expression.
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GLI2 Transcriptional Cascade During Mouse Fetal Lung DevelopmentRutter, Martin Edward 01 August 2008 (has links)
The lung is an organ that contains a vast system of airways carefully constructed to achieve maximal surface area in a confined space, requiring guidance from a multitude of developmental factors. The Shh pathway is one such signaling mechanism that is critical to proper lung formation, guiding branching morphogenesis and cellular proliferation through its downstream Gli transcription factors. Additionally, Foxf1 has been shown to be a key developmental factor required for proper lung formation during embryogenesis. Although theorized that the Gli transcription factors are responsible for regulating foxf1 levels, their exact relationship has yet to be revealed. Using five different models for Shh signaling (gli2 null, gli2 over-expressor [hVER-Gli2], gli3 null, Gli3 constitutive repressor [Gli3Δ699] and cyclopamine treated lung explants), I compared and contrasted the role of Gli2 and Gli3 in terms of their effect on cell cycle regulation, and on the expression levels of foxf1 and its potential downstream target genes tbx4, tbx5 and fgf10. I found that ectopic over-expression of gli2 resulted in increased Shh pathway activation, and increased expression of G1/S phase cyclins, which was associated with increased cellular proliferation and lung growth. However, no change in the levels of G1/S phase cyclins due to altered Gli3 signaling was observed. Foxf1 levels positively correlate with the levels of gli2, and appear to be independent of Gli3 activity. The amount of tbx4, tbx5, and fgf10 transcripts were observed to follow the levels of gli2 in the different gli2 mouse models, however, there was no significant change in gli3 null or Gli3Δ699 mice. Finally, by analyzing gene expression at different time points during gestation, I found that while gli2 levels affect foxf1 throughout gestation, the relationship to tbx4, tbx5 and fgf10, occurs only during the latter stages of lung development. I conclude, that Gli2 and not Gli3 appears to be the primary transducer of Shh signaling influencing cyclin regulation, leading to changes in embryonic lung growth. Furthermore, that Gli2 and not Gli3 appears to regulate foxf1 expression levels, and that this may extend downstream to influence tbx4, tbx5 and fgf10 expression.
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Cellular dynamics in Zebrafish optic cup morphogenesisSidhaye, Jaydeep 22 January 2018 (has links) (PDF)
Organ formation is an important step during development of an organism that combines different scales from the molecular to the tissue level. Many organogenesis phenomena involve epithelial morphogenesis, where sheets of cells undergo rearrangements to form complex architectures – organ precursors, which subsequently develop into mature organs. Timely development of the characteristic architectures of the organ precursors is crucial for successful organogenesis and is determined by the choice of epithelial rearrangements that organise the constituent cells in space and time. However, for many organogenesis events the cellular dynamics underlying such epithelial rearrangements remain elusive.
In the work presented here, I investigated the morphogenesis of the hemispherical retinal neuroepithelium (RNE), that serves as an organ precursor of the neural retina. Formation of RNE is an important event in vertebrates that shapes the optic cup and sets the stage for subsequent eye development. I investigated RNE morphogenesis in the developing zebrafish embryo by visualising and investigating the cellular dynamics of the process in vivo. My findings show that the zebrafish RNE is shaped by the combined action of two different epithelial rearrangements – basal shrinkage of the neuroepithelial cells and involution of cells at the rim of the developing optic cup. The basal shrinkage of the neuroepithelial cells bends the neuroepithelial sheet and starts the process of invagination. However, my results show that the major player in RNE morphogenesis is rim involution. Rim involution translocates prospective RNE cells to their designated location in the invaginating layer and contributes to RNE invagination. My work unravelled the so far unknown mechanism of rim involution. I show that the rim cells involute by collective epithelial migration using directed membrane protrusions and dynamic cell-matrix contacts. If rim migration is perturbed, the prospective RNE cells cannot reach the invaginating layer. As a result, these migration-defective cells attain the RNE fate at an ectopic location and disrupt the tissue architecture. Therefore, rim migration coordinates the cellular location with the timing of RNE fate determination and orchestrates RNE morphogenesis in space and time. Overall, my work highlights how morphogenetic processes shape the organ precursor architecture and ensure timely organ formation. These findings provide important insights not only for eye development but also for epithelial morphogenesis and organogenesis in many other systems. / Für die Entwicklung eines Organismus ist die Bildung von Organen (Organogenese) von zentraler Bedeutung. Organogenese umfasst Prozesse auf allen Ebenen der Längenskala: von der molekularen Ebene, der Gewebeebene, bis hin zur Ebene des ganzen Organismus. Viele Phänomene der Organogenese beinhalten dabei Veränderungen von Epithelien, bei der sich Schichten von Zellen zu komplexen Strukturen - Organvorläufern - umwandeln. Diese entwickeln sich später zu vollständigen Organen. Die rechtzeitige Entwicklung der charakteristischen Architektur der Organvorläufer ist entscheidend für eine erfolgreiche Organogenese und wird durch die Wahl der epithelialen Umwandlungsprozessen bestimmt, welche die Zellen in Raum und Zeit koordinieren müssen. Für viele dieser Prozesse ist jedoch genau diese zugrundeliegende Zelldynamik unklar.
In der hier vorgestellten Arbeit untersuchte ich die Bildung des hemisphärischen retinalen Neuropepithels (RNE). Das RNE ist der Organvorläufer der neuralen Retina, weshalb dessen korrekte Bildung die Voraussetzung für die korrekte Entwicklung der Augen ist. Ich untersuchte die RNE-Morphogenese in sich entwickelnden Zebrafisch-Embryos durch Visualisierung und Untersuchung der zellulären Dynamik der beteiligten Prozesse in vivo. Meine Ergebnisse zeigen, dass das RNE in Zebrafischen durch die kombinierte Umwandlung von zwei verschiedenen Epithelien geformt wird. Zum einen findet eine Verkleinerung des basalen Prozesses der neuroepithelialen Zellen statt, zum anderen die Involution von Randzellen. Die basale Verkleinerung der neuroepithelialen Zellen verbiegt die neuroepitheliale Schicht und führt zur Einstülpung des RNE. Meine Ergebnisse zeigten allerdings, dass Involution von Randzellen noch bedeutsamer für die RNE-Morphogenese ist. Die involution von Randzellen transportiert potenzielle RNE-Zellen in das Neuroepithel und trägt zur RNE-Einstülpung bei. Die Bedeutung meiner Arbeit liegt darin, den bisher unbekannten Mechanismus der Randzell-Involution entdeckt zu haben. Ich zeigte, dass die Randzellen sich aktiv durch kollektive epitheliale Migration bewegen indem sie gerichtete Membranforsätze und dynamische Zell zu Matrix Kontakte etablieren. Wird die Migration der Randzellen inhibiert, so führt dies dazu, dass diese Zellen die eingestülpte RNE Schicht nicht erreichen. Sie landen dann an den falschen Positionen, wo sie die Gewerbearchitektur stören können. Daher koordiniert die Randzellmigration die Position der Zellen und orchestriert die RNE-Morphogenese in Raum und Zeit. Insgesamt zeigt meine Arbeit, wie morphogenetische Prozesse die Organvorläuferarchitektur prägen und eine rechtzeitige Organbildung sicherstellen. Diese Erkenntnisse sind sowohl für das Verständnis der Augenentwicklung, als auch für das der epithelialen Morphogenese und Organogenese in anderen Systemen von großer Bedeutung.
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Cellular dynamics in Zebrafish optic cup morphogenesisSidhaye, Jaydeep 07 December 2017 (has links)
Organ formation is an important step during development of an organism that combines different scales from the molecular to the tissue level. Many organogenesis phenomena involve epithelial morphogenesis, where sheets of cells undergo rearrangements to form complex architectures – organ precursors, which subsequently develop into mature organs. Timely development of the characteristic architectures of the organ precursors is crucial for successful organogenesis and is determined by the choice of epithelial rearrangements that organise the constituent cells in space and time. However, for many organogenesis events the cellular dynamics underlying such epithelial rearrangements remain elusive.
In the work presented here, I investigated the morphogenesis of the hemispherical retinal neuroepithelium (RNE), that serves as an organ precursor of the neural retina. Formation of RNE is an important event in vertebrates that shapes the optic cup and sets the stage for subsequent eye development. I investigated RNE morphogenesis in the developing zebrafish embryo by visualising and investigating the cellular dynamics of the process in vivo. My findings show that the zebrafish RNE is shaped by the combined action of two different epithelial rearrangements – basal shrinkage of the neuroepithelial cells and involution of cells at the rim of the developing optic cup. The basal shrinkage of the neuroepithelial cells bends the neuroepithelial sheet and starts the process of invagination. However, my results show that the major player in RNE morphogenesis is rim involution. Rim involution translocates prospective RNE cells to their designated location in the invaginating layer and contributes to RNE invagination. My work unravelled the so far unknown mechanism of rim involution. I show that the rim cells involute by collective epithelial migration using directed membrane protrusions and dynamic cell-matrix contacts. If rim migration is perturbed, the prospective RNE cells cannot reach the invaginating layer. As a result, these migration-defective cells attain the RNE fate at an ectopic location and disrupt the tissue architecture. Therefore, rim migration coordinates the cellular location with the timing of RNE fate determination and orchestrates RNE morphogenesis in space and time. Overall, my work highlights how morphogenetic processes shape the organ precursor architecture and ensure timely organ formation. These findings provide important insights not only for eye development but also for epithelial morphogenesis and organogenesis in many other systems. / Für die Entwicklung eines Organismus ist die Bildung von Organen (Organogenese) von zentraler Bedeutung. Organogenese umfasst Prozesse auf allen Ebenen der Längenskala: von der molekularen Ebene, der Gewebeebene, bis hin zur Ebene des ganzen Organismus. Viele Phänomene der Organogenese beinhalten dabei Veränderungen von Epithelien, bei der sich Schichten von Zellen zu komplexen Strukturen - Organvorläufern - umwandeln. Diese entwickeln sich später zu vollständigen Organen. Die rechtzeitige Entwicklung der charakteristischen Architektur der Organvorläufer ist entscheidend für eine erfolgreiche Organogenese und wird durch die Wahl der epithelialen Umwandlungsprozessen bestimmt, welche die Zellen in Raum und Zeit koordinieren müssen. Für viele dieser Prozesse ist jedoch genau diese zugrundeliegende Zelldynamik unklar.
In der hier vorgestellten Arbeit untersuchte ich die Bildung des hemisphärischen retinalen Neuropepithels (RNE). Das RNE ist der Organvorläufer der neuralen Retina, weshalb dessen korrekte Bildung die Voraussetzung für die korrekte Entwicklung der Augen ist. Ich untersuchte die RNE-Morphogenese in sich entwickelnden Zebrafisch-Embryos durch Visualisierung und Untersuchung der zellulären Dynamik der beteiligten Prozesse in vivo. Meine Ergebnisse zeigen, dass das RNE in Zebrafischen durch die kombinierte Umwandlung von zwei verschiedenen Epithelien geformt wird. Zum einen findet eine Verkleinerung des basalen Prozesses der neuroepithelialen Zellen statt, zum anderen die Involution von Randzellen. Die basale Verkleinerung der neuroepithelialen Zellen verbiegt die neuroepitheliale Schicht und führt zur Einstülpung des RNE. Meine Ergebnisse zeigten allerdings, dass Involution von Randzellen noch bedeutsamer für die RNE-Morphogenese ist. Die involution von Randzellen transportiert potenzielle RNE-Zellen in das Neuroepithel und trägt zur RNE-Einstülpung bei. Die Bedeutung meiner Arbeit liegt darin, den bisher unbekannten Mechanismus der Randzell-Involution entdeckt zu haben. Ich zeigte, dass die Randzellen sich aktiv durch kollektive epitheliale Migration bewegen indem sie gerichtete Membranforsätze und dynamische Zell zu Matrix Kontakte etablieren. Wird die Migration der Randzellen inhibiert, so führt dies dazu, dass diese Zellen die eingestülpte RNE Schicht nicht erreichen. Sie landen dann an den falschen Positionen, wo sie die Gewerbearchitektur stören können. Daher koordiniert die Randzellmigration die Position der Zellen und orchestriert die RNE-Morphogenese in Raum und Zeit. Insgesamt zeigt meine Arbeit, wie morphogenetische Prozesse die Organvorläuferarchitektur prägen und eine rechtzeitige Organbildung sicherstellen. Diese Erkenntnisse sind sowohl für das Verständnis der Augenentwicklung, als auch für das der epithelialen Morphogenese und Organogenese in anderen Systemen von großer Bedeutung.
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Genetic And Biochemical Studies On Genes Involved In Leaf MorphogenesisAggarwal, Pooja 02 1900 (has links)
Much is known about how organs acquire their identity, yet we are only beginning to learn how their shape is regulated. Recent work has elucidated the role of coordinated cell division & expansion in determining plant organ shape. For instance, in Antirrhinum, leaf shape is affected in the cincinnata (cin) mutant because of an alteration in the cell division pattern. CIN codes for a TCP transcription factor and controls cell proliferation. It is unclear how exactly CIN-like genes regulate leaf morphogenesis. We have taken biochemical and genetic approach to understand the TCP function in general and the role of CIN-like genes in leaf morphogenesis in Antirrhinum and Arabidopsis.
Targets of CINCINNATA
To understand how CIN controls Antirrhinum leaf shape, we first determined the consensus target site of CIN as GTGGTCCC by carrying out RBSS assay. Mutating each of this target sequence, we determined the core binding sequence as TGGNCC. Hence, all potential direct targets of CIN are expected to contain a TGGNCC sequence.
Earlier studies suggested that CIN activates certain target genes that in turn repress cell proliferation. To identify these targets, we compared global transcripts of WT and cin leaves by differential display PCR and have identified 18 unique, differentially expressed transcripts. To screen the entire repertoire of differentially expressed transcripts, we have carried out extensive micro-array analysis using 44K Arabidopsis chips as well as 13K custom-made Antirrhinum chips. Combining the RBSS data with the results obtained from the micro-array experiments, we identified several targets of CIN. In short, CIN controls expression of the differentiation-specific genes from tip to base in a gradient manner. In cin, such gradient is delayed, thereby delaying differentiation. We also find that gibberellic acid, cytokinin and auxin play important role in controlling leaf growth.
Genetic characterization of CIN-homologues in Arabidopsis
Arabidopsis has 24 TCP genes. Our work and reports from other groups have shown that TCP2, 4 and 10 are likely to be involved in leaf morphogenesis. These genes are controlled by a micro RNA miR319. To study the role of TCP4, the likely orthologue of CIN, we generated both stable and inducible RNAi lines. Down-regulation of TCP4 transcript resulted in crinkly leaves, establishing the role of TCP4 in leaf shape. To study the function of TCP2, 4 & 10 in more detail, we isolated insertion mutants in these loci. The strongest allele of TCP4 showed embryonic lethal phenotype, indicating a role for TCP4 in embryo growth. All other mutants showed mild effect on leaf shape, suggesting their redundant role. Therefore, we generated and studied various combinations of double and triple mutants to learn the concerted role of these genes on leaf morphogenesis.
To further study the role of TCP4 in leaf development, we generated inducible RNAi and miRNA-resistant TCP4 transgenic lines and carried out studies with transient down-regulation and up-regulation of TCP4 function. Upon induction, leaf size increased in RNAi transgenic plants whereas reduced drastically in miR319 resistant lines, suggesting that both temporal & spatial regulation of TCP4 is required for leaf development.
Biochemical characterization of TCP domain
To study the DNA-binding properties of TCP4, random binding site selection assay (RBSS) was carried out and it was found that TCP4 binds to a consensus sequence of GTGGTCCC. By patmatch search and RT-PCR analysis, we have shown that one among 74 putative targets, EEL (a gene involved in embryo development), was down regulated in the RNAi lines of TCP4. This suggests that EEL could be the direct target of TCP4. We have tested this possibility in planta by generating transgenic lines in which GUS reporter gene is driven by EEL upstream region with either wild type or mutated TCP4 binding site. GUS analysis of embryos shows that transgenic with mutated upstream region had significantly reduced reporter activity in comparison to wild type, suggesting that EEL is a direct target of TCP4. We have further shown that TCP4 also binds to the upstream region of LOX2, a gene involved in Jasmonic acid (JA) biosynthesis (in collaboration with D. Weigel, MPI, Tubingen, Germany).
TCP domain has a stretch of basic residues followed by a predicted helix-loop-helix region (bHLH), although it has little sequence homology with canonical bHLH proteins. This suggests that TCP is a novel and uncharacterized bHLH domain. We have characterized DNA-binding specificities of TCP4 domain. We show that TCP domain binds to the major groove of DNA with binding specificity comparable to that of bHLH proteins. We also show that helical structure is induced in the basic region upon DNA binding. To determine the amino acid residues important for DNA binding, we have generated point mutants of TCP domain that bind to the DNA with varied strength. Our analysis shows that the basic region is important for DNA binding whereas the helix-loop-helix region is involved in dimerization. Based on these results, we have generated a molecular model for TCP domain bound to DNA (in Collaboration with Prof. N. Srinivasan, IISc, Bangalore). This model was validated by further site-directed mutagenesis of key residues and in vitro assay.
Functional analysis of TCP4 in budding yeast
To assess TCP4 function in regulation of eukaryotic cell division, we have introduced TCP4 in S. cerevisiae under the GAL inducible promoter. TCP4 induction in yeast cells always slowed down its growth, indicative of its detrimental effect on yeast cell division. Flow cytometry analysis of synchronized cells revealed that TCP4 arrests yeast cell division specifically at G1→S boundary. Moreover, induced cells showed distorted cell morphology resembling shmoo phenotype. Shmooing is a developmental process which usually happened when the haploid cells get exposed to the cells of opposite mating type and get arrested at late G1 phase due to the inhibition of cdc28-cln2 complex. This suggested that TCP4-induced yeast cells are arrested at late G1 phase probably by the inhibition of cdc28-cln2 complex. To further investigate how TCP4 induce G1→S arrest, we carried out microarray analysis and found expression of several cell cycle markers significantly altered in TCP4-induced yeast cells.
Studies on crinkly1, a novel leaf mutant in Arabidopsis
To identify new genes involved in leaf morphogenesis, we have identified crinkly1 (crk1), a mutant where leaf shape and size are altered. We observed that crk1 also makes more number of leaves compared to wild type. Phenotypic analysis showed that crk1 leaf size is ~5 times smaller than that of wild type. Scanning electron microscopy (SEM) showed that both cell size and number are reduced in the mutant leaf, which explains its smaller size. We have mapped CRK1 within 3 cM on IV chromosome.
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Information driven self-organization of agents and agent collectivesHarder, Malte January 2014 (has links)
From a visual standpoint it is often easy to point out whether a system is considered to be self-organizing or not, though a quantitative approach would be more helpful. Information theory, as introduced by Shannon, provides the right tools not only quantify self-organization, but also to investigate it in relation to the information processing performed by individual agents within a collective. This thesis sets out to introduce methods to quantify spatial self-organization in collective systems in the continuous domain as a means to investigate morphogenetic processes. In biology, morphogenesis denotes the development of shapes and form, for example embryos, organs or limbs. Here, I will introduce methods to quantitatively investigate shape formation in stochastic particle systems. In living organisms, self-organization, like the development of an embryo, is a guided process, predetermined by the genetic code, but executed in an autonomous decentralized fashion. Information is processed by the individual agents (e.g. cells) engaged in this process. Hence, information theory can be deployed to study such processes and connect self-organization and information processing. The existing concepts of observer based self-organization and relevant information will be used to devise a framework for the investigation of guided spatial self-organization. Furthermore, local information transfer plays an important role for processes of self-organization. In this context, the concept of synergy has been getting a lot attention lately. Synergy is a formalization of the idea that for some systems the whole is more than the sum of its parts and it is assumed that it plays an important role in self-organization, learning and decision making processes. In this thesis, a novel measure of synergy will be introduced, that addresses some of the theoretical problems that earlier approaches posed.
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Genetic analysis of a signal transduction pathway : the regulation of invasive growth and starch degradation in Saccharomyces cerevisiaeVan Dyk, Dewald, 1975- 03 1900 (has links)
Dissertation (PhD)--University of Stellenbosch, 2004. / ENGLISH ABSTRACT: Cells of the yeast Saccharomyces cerevisiae are able to change their morphological
appearance in response to a variety of extracellular and intracellular signals. The
processes involved in morphogenesis are well characterised in this organism, but the
exact mechanism by which information emanating from the environment is integrated into
the regulation of the actin cytoskeleton and the yeast cell cycle, is still not clearly
understood. Considerable progress has, however, been made. The processes are
investigated on various levels including: (i) the nature of the signals required to elicit a
morphological adaptation, (ii) the mechanism by which these signals are perceived and
transmitted to the nucleus for gene transcription regulation (signal transduction pathways),
(iii) the role of the cytoskeleton, particularly actin, in morphogenesis, and (iv) the
relationship between cell cycle regulators and factors required for alterations in cellular
shape.
The focus of this study was on elements involved in the regulation of one of these
morphological processes, pseudohyphal formation, in S. cerevisiae. During pseudohyphal
differentiation normal oval yeast cells become elongated and mother and daughter cells
stay attached after cytokinesis to give rise to filaments. These filaments are able to
penetrate the growth substrate, a phenomenon referred to as invasive growth. Actin
remodelling is a prerequisite for the formation of elongated cells during pseudohyphal
development and invasive growth. Its main contribution to this event is the directing of
vesicles, containing cell wall constituents and enzymes, to specific sites of cell wall growth
at the cell periphery. In order to fulfil this cellular function, actin is regulated on several
levels. Signal transduction pathways that are activated in response to external nutritional
signals play important roles in the regulation of the actin cytoskeleton during pseudohyphal
differentiation. For this reason a literature review was compiled to introduce various
aspects of actin-structure, the regulation of this structure and the functions actin performs
during morphogenesis. The connection between signal transduction elements involved in
morphological processes and actin remodelling is also reviewed.
This study entailed the genetic analysis of numerous factors involved in the
regulation of pseudohyphal differentiation, invasive growth and starch metabolism. Several
transcriptional regulators playing a role in these phenomena were investigated. Apart from
the transcription factors, which include Mss11p, Msn1p, Ste12p, F108p,Phd1p and Tec1p,
additional elements ranging from transporters to G-proteins, were also investigated.
Mutant strains deleted for one or more of these factors were constructed and tested to
assess their abilities to form filaments that penetrate the growth substrate, and to utilise
starch as a carbon source. Complex genetic relationships were observed for various
combinations of these factors. Specifically, F108p,Msn1p and Ste12p were shown to act
independently in controlling invasive growth and starch metabolism, suggesting that these
factors are regulated by different signal transduction pathways. Mss11p, on the other hand, was found to play an indispensable role and seems to act as a downstream factor of
Msn1 p, Fl08p, Ste12p and Tec1 p. The exception to this is Phd1 p, since multiple copies of
PHD1 partially suppress the effect of a MSS11 deletion. The data suggests that Mss11 p
functions at the confluence of several signalling pathways controlling the transcriptional
regulation of genes required for invasive growth and starch degradation.
Different nutritional signals were also found to differentially regulate specific
signalling elements during the invasive growth response. For example, Tec1 p requires
Msn1 p activity in response to growth on media containing a limited nitrogen source. This
dependency, however, was absent when invasive growth was tested on glucose and
starch media.
Evidence was also obtained that confirmed the transcriptional co-regulation of
MUC1 and STA2. MUC1 encodes a mucin-like protein that is required for invasive growth
and pseudohyphal differentiation, whereas STA2 encodes a glucoamylase required for
starch degradation. Unpublished results indicated that several transcriptional regulators of
invasive growth also exert an effect on starch metabolism. The data generated during this
study complemented and confirmed published results. It also contributed to the
compilation of a more detailed model, integrating the numerous factors involved in these
signalling processes. / AFRIKAANSE OPSOMMING: Saccharomyces cerevisiae gisselle beskik oor die vermoë om hul morfologiese voorkoms
in responstot 'n verskeidenheid van ekstrasellulêre en intrasellulêre seine te verander. Die
prosesse betrokke by morfogenese is goed gekarakteriseerd in hierdie organisme, maar
die presiese meganisme waardeur inligting vanuit die omgewing geïntegreer word in die
reguleringvan die aktien-sitoskelet en die gisselsiklus, word nog nie ten volle verstaan nie.
Aansienlike vordering in die verband is egter gemaak. Die prosesse word op verskeie
vlakke ondersoek, insluitende: (i) die aard van die seine wat benodig word om 'n
morfologiese aanpassing te inisïeer; (ii) die meganisme waardeur hierdie seine
waargeneem en herlei word na die selkern vir die regulering van geen-transkripsie
(seintransduksie paaie); (iii) die rol van die sitoskelet, spesifiek aktien, in morfogenese en
(iv) die verhouding tussen selsiklusreguleerders en faktore wat benodig word vir
verandering in selvorm.
Hierdie navorsing fokus op elemente betrokke by die regulering van een van hierdie
morfologiese prosesse in S. cerevisiae, naamlik pseudohife-vorming. Gedurende
pseudohife-differensiëring neem tipiese ovaalvormige selle 'n verlengde voorkoms aan wat
tot die vorming van filamente lei. Hierdie filamente is in staat om die groeisubstraat te
penetreer, 'n verskynsel bekend as penetrasie-groei. Aktienherrangskikking is 'n
voorvereiste vir die vorming van verlengde selle tydens pseudohife-ontwikkeling. Die
hoofbydrae van aktien tot hierdie verskynsel is die oriëntering van uitskeidingsvesikels,
wat selwandkomponente en ensieme bevat, na spesifieke areas van selwandgroei op die
seloppervlak. Aktien word op verskeie vlakke gereguleer om hierdie sellulêre funksie te
vervul. Seintransduksiepaaie wat geaktiveer word in respons tot ekstrasellulêre
voedingsseine speel 'n belangrike rol in die regulering van die aktien-sitoskelet tydens
pseudohife-differensiëring. Op grond hiervan is 'n literatuuroorsig saamgestel vir die
bekendstelling van verskeie aspekte van aktienstruktuur, die regulering van hierdie
strukture en die funksies wat deur aktien gedurende morfogenese vervul word. Die
verband tussen seintransduksie-elemente betrokke by morfologiese prosesse en aktien
herrangskikkingword ook behandel.
Hierdie studie het die genetiese analisering van verskeie faktore betrokke by
pseudohife-differensiëring, penetrasie-groei en styselmetabolisme, behels. Verskeie
transkripsionele reguleerders wat In rol speel in hierdie prosesse was bestudeer. Buiten
die transkripsiefaktore Mss11p, Msn1p, Ste12p, F108p,Phd1P en Tec1p, was addisionele
faktore, wat gewissel het van transporters tot G-proteïene, ook ondersoek. Mutante-rasse
met geendelesies vir een of meer van hierdie faktore is gekonstrueer en getoets om vas te
stel hoe dit hul vermoë raak om penetrerende filamente te vorm, asook om te bepaal of
stysel as koolstofbron gebruik kan word. Komplekse genetiese interaksies vir verskeie
kombinasies van hierdie faktore is waargeneem. Dit was waargeneem dat F108p,Msn1p en Ste12p onafhanklik funksioneer tydens die regulering van penetrasie-groei en
styselmetabolisme, wat impliseer dat hierdie faktore deur verskillende
seintransduksiepaaie gereguleer word. Mss11 p word beskou as In onmisbare rolspeler in
hierdie prosesse en dit kom voor asof hierdie protein as 'n stroom-af faktor is en vereis
word vir die funksionering van Msn1p, F108p, Ste12p en Tec1p. Phd1p is egter 'n
uitsondering, aangesien veelvuldige kopieë van PHD1 die effek van 'n MSS11-delesie
gedeeltelik oorkom. Die data impliseer dat Mss11 p by die samevloei van verskeie
seintransduksiepaaie, benodig vir die transkripsionele regulering van gene betrokke by
penetrasie-groei en styselmetabolisme, funksioneer.
Dit was ook waargeneem dat verskillende voedingsseine die faktore betrokke by die
penetrasie-groeirespons differensieel reguleer. Tec1 p byvoorbeeld benodig Msn1paktiwitieit
in respons tot groei op media met 'n beperkte stikstofbron. Hierdie afhanklike
interaksie is egter afwesig wanneer penetrasie-groei bestudeer word op glukose- en
styselmedia.
Resultate wat die gesamentlike transkripsionele regulering van MUC1 en STA2
bevestig, is ook verkry. MUC1 kodeer vir 'n mukienagtige proteïen wat benodig word vir
pseudohife-vorming en penetrasie-groei, terwyl STA2 kodeer vir 'n glukoamilase
essensieël vir styselafbraak. Ongepubliseerde resultate dui daarop dat verskeie
transkripsionele reguleerders van penetrasie-groei ook In effek uitoefen op
styselmetabolisme. Die data wat gegenereer is tydens hierdie studie komplementeer en
bevestig reeds gepubliseerde resultate. Dit het ook bygedra tot die samestelling van 'n
gedetaileerde model wat die verskillende faktore, betrokke by hierdie
seintransduksieprosesse, integreer.
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