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Thesis (Ph. D.)--University of Washington, 2006. / Vita. Includes bibliographical references (leaves 109-117).

Marine microbes support global carbon cycling by sequestration and metabolizing of marine carbon. Understanding how these microbes use unique motility modalities to navigate the physicochemical environment of the ocean is crucial to understanding microbial carbon metabolism. Motility in several marine Rhodobacter strains exhibit dendritic motility, but underlying genetic mechanisms remain poorly characterized. To lay groundwork for future study of genetic mechanisms for dendritic motility in novel Rhodobacter strains HOT5_B8 and HOT5_C3, we use timelapse microscopy to qualitatively and quantitatively characterize patterns in dendrite formation. Preliminary results determine that dendritic motility is faster than non-dendritic motility in HOT5_B8 and HOT5_C3. Further, key differences in HOT5_B8 and HOT5_C3 behaviors are used as evidence to posit putative density-dependent mechanisms in the formation and behaviors of dendrites. / 2023-09-10T00:00:00Z

Thesis (Ph. D.)--West Virginia University, 2002. / Title from document title page. Document formatted into pages; contains vii, 218 p. : ill. (some col.). Vita. Includes abstract. Includes bibliographical references.

Reproduction de : Thèse de doctorat : Médecine. Neurobiologie : Nantes : 2009. / Bibliogr.

Thesis (Ph.D.)--Boston University / PLEASE NOTE: Boston University Libraries did not receive an Authorization To Manage form for this thesis or dissertation. It is therefore not openly accessible, though it may be available by request. If you are the author or principal advisor of this work and would like to request open access for it, please contact us at open-help@bu.edu. Thank you. / A fundamental aspect of vision is the ability to detect motion and to define its direction. In the retina, directionally selective ganglion cells respond to stimulus motion in a 'preferred' direction but respond little to stimulus motion in the opposite or 'null' direction. However despite nearly forty years of investigation, the precise cellular locus and underlying mechanisms of direction selective encoding have remained largely elusive. Recently, starburst amacrine cells, that are presynaptic to directionally selective ganglion cells, have been shown to provide direction specific inhibitory output to these ganglion cells. Therefore defining the biophysical properties specific to starburst amacrine cell dendrites will provide significant insight into the ability of visual systems to encode the direction of objects moving through an animal's visual field. Using a combination of intracellular filling of starburst amacrine cells and immunohistochemical localization of biophysically relevant molecules, we have examined how individual dendrites compute such motion. In order to define the relative degree and pattern of colocalization of these markers on filled dendrites we developed a new set of image acquisition and data analysis procedures that have allowed us to define the biophysical signature intrinsic to different portions of starburst amacrine cell dendrites. We have found that sodium-potassium-chloride cotransporter (NKCC2) and potassium-chloride cotransporter (KCC2) are expressed and differentially distributed on the proximal and distal dendritic compartments of starburst amacrine cells, respectively. The functional relevance of the anatomical distribution pattern of these cation-chloride-cotransporter types has been confirmed by others using physiological techniques. In summary, our studies provide a fundamental mechanism through which starburst amacrine cells define motion direction and transmit this information to directionally selective ganglions cells. In addition, our illumination of the basic concept of segregation of functional components to different dendritic compartments will likely prove to be an important theme of neuronal function throughout the nervous system. / 2031-01-01

No description available.

Fibroblast growth factor 2 (FGF-2) is known to be released from cartilage upon injury and is able to influence chondrocyte gene expression in vitro. In cartilage, FGF-2 regulates E11/podoplanin expression in murine joints following surgical destabilisation (DMM model of osteoarthritis (OA)), and in cartilage explant injury models. In bone, E11 is critical for the early stages of osteocytogenesis and is responsible for the acquisition of the osteocyte dendritic phenotype. This dendritic phenotype is dysregulated in OA and given the known role of the osteocyte in controlling bone remodelling, this may contribute to the subchondral bone thickening observed in OA. Hence, the aim of this study was to elucidate the nature of FGF-2- mediated E11 expression and osteocytogenesis in skeletal health and disease. This thesis has shown that FGF-2 dose-dependently increased E11 mRNA expression in MC3T3 cells, primary osteoblasts and in primary calvaria organ cultures, which was confirmed by E11 protein western blotting data. The FGF-2 induced changes in E11 expression were accompanied by significant increases in the mRNA expression of the osteocyte markers Phex and Dmp1, and significant decreases in the mRNA expression of the osteoblast markers Col1a1, Postn, Bglap and Alpl expression. This thus supports the hypothesis that FGF-2 drives osteocytogenesis. The acquisition of osteocyte phenotype involves the re-organisation of the cytoskeleton, such as F-actin. This step is important for the transition of cuboidal-shaped osteoblasts to the stellate-shaped osteocyte phenotype. FGF-2 stimulation of MC3T3 cells and primary osteoblasts revealed more numerous and longer dendrites, as visualised by phalloidin staining for F-actin and indicative of the acquisition of the osteocyte phenotype. In contrast, control cells had a typical rounded morphology with fewer and shorter dendrites. Furthermore, immunofluorescence labelling for E11 in control cells revealed uniform distribution throughout the cytoplasm, especially in the perinuclear region. In contrast, FGF-2 treated cells showed a modified distribution where E11 was negligible in the cytoplasm, but concentrated in the dendrites. The use of siRNA knockdown of E11 achieved a 70% reduction of basal E11 mRNA expression. This knockdown also effectively abrogated FGF-2-related changes in E11 expression and dendrite formation as disclosed by mRNA and protein expression, immunofluorescence and F-actin staining with phalloidin. Despite these FGF-2 driven increases in E11 and osteocyte dendrite formation in vitro, immunohistochemical labelling revealed no differences in E11 expression in subchondral, trabecular and cortical osteocytes from naïve Fgf-2 deficient mice in comparison to wild-type mice. Similar results were observed upon sclerostin immunolabelling. FGF-2 stimulation of MC3T3 cells elicited activation of ERK1/2, Akt and p38 MAPK. However, inhibition of the aforementioned pathways failed to reduce FGF-2- mediated E11 expression and as such, the specific signalling pathway responsible remains unclear. Upstream, the expression of Fgfr1 was increased (>10-fold) over 24 h time point, while a reduction was seen in Fgfr2/3 expression over same time point especially in the FGF-2 treated cultures. This suggests that increased E11 expression and the acquisition of the osteocyte phenotype may be speculatively though upregulation of Fgfr1. The expression of E11 and sclerostin in OA pathology in mice, human and dogs were investigated. Initially sequence homology using the Clustal Omega alignment program showed both proteins to be homologous in the domestic animals under study. A comparative study using canine subchondral bone osteocytes revealed increased E11 expression in the OA samples relative to the control. This feature may be related to newly embedded osteocytes during sclerosis. However, E11 and sclerostin were unchanged in both murine (DMM) and human OA subchondral bone osteocytes in comparison to controls. In mice, this may be due to limited OA development; whilst in humans the sample size, age, stage of the disease and sourcing from same diseased joint may be important in the interpretation of the results. The expression of E11 and sclerostin during OA pathology was also investigated in Fgf-2 deficient mice in which OA was induced using the DMM model. There was no difference in E11 expression between the OA and control (sham-operated) samples, suggesting that compensation of E11 expression may be mediated by growth factors from the FGF family. Surprisingly, increased E11 expression was observed in the control Fgf-2 deficient mice, in comparison to the wild-type control mice. This suggests a potential adjustment to loading by the contralateral knee, as this was not observed in naïve mice from both groups. Together, these data show that FGF-2 promotes the osteocyte phenotype, and that this is mediated by increased E11 expression. These results may help explain (1) the altered osteocyte phenotype and (2) increased subchondral bone thickening observed in OA. This knowledge will be of interest in the search for disease modifying therapeutics for skeletal health, including OA and osteoporosis.