No description available.

During C. elegans embryogenesis, myoblasts initially form two rows along the left and right lateral midlines and at ~290 min of development migrate dorsally and ventrally to form the four muscle quadrants present upon hatching (Sulston et al, 1983). As the myoblasts migrate they are still dividing, as are many other cells in their immediate environment. This means the cell-cell contact of cells during migration is dynamic and can vary from animal to animal (Schnabel et al, 1997). This situation creates an environment where the extracellular matrix (ECM) and cell surface contacts are in constant flux, which begs the questions as to how these cells navigate unerringly to their final destination. In an attempt to identify genes mediating these migrations, I performed an RNAi based screen targeting 776 genes predicted to be members of the extracellular matrix (ECM), or one of its receptors. Using both feeding and injection based RNAi, I was able to identify three genes of interest. Knockdowns of F56B3.2 resulted in paralyzed animals with detached muscle, making it a good candidate for a new component of the muscle attachment complex. F33G12.4 knockdowns resulted in an embryonic arrest phenotype with an abnormal muscle lineage, possibly stemming from polarity defects. The only knockdown that resulted in muscle migration defects was that for lam-2, which encodes for the laminin gamma subunit. Analysis of the lam-2 knockdown, as well as knockdowns for the other laminin subunits, revealed dorsal/ventral migration defects as well as a posterior displacement of the anterior-most ventral muscle cells. Investigation of this posterior displacement has led to the identification of a previously un-described anterior muscle migration event and its dependency upon the extension of muscle processes from the leading cells.

During C. elegans embryogenesis, myoblasts initially form two rows along the left and right lateral midlines and at ~290 min of development migrate dorsally and ventrally to form the four muscle quadrants present upon hatching (Sulston et al, 1983). As the myoblasts migrate they are still dividing, as are many other cells in their immediate environment. This means the cell-cell contact of cells during migration is dynamic and can vary from animal to animal (Schnabel et al, 1997). This situation creates an environment where the extracellular matrix (ECM) and cell surface contacts are in constant flux, which begs the questions as to how these cells navigate unerringly to their final destination. In an attempt to identify genes mediating these migrations, I performed an RNAi based screen targeting 776 genes predicted to be members of the extracellular matrix (ECM), or one of its receptors. Using both feeding and injection based RNAi, I was able to identify three genes of interest. Knockdowns of F56B3.2 resulted in paralyzed animals with detached muscle, making it a good candidate for a new component of the muscle attachment complex. F33G12.4 knockdowns resulted in an embryonic arrest phenotype with an abnormal muscle lineage, possibly stemming from polarity defects. The only knockdown that resulted in muscle migration defects was that for lam-2, which encodes for the laminin gamma subunit. Analysis of the lam-2 knockdown, as well as knockdowns for the other laminin subunits, revealed dorsal/ventral migration defects as well as a posterior displacement of the anterior-most ventral muscle cells. Investigation of this posterior displacement has led to the identification of a previously un-described anterior muscle migration event and its dependency upon the extension of muscle processes from the leading cells.

Thesis (Ph. D.)--School of Biological Sciences. University of Missouri--Kansas City, 2007. / "A dissertation in molecular biology and biochemistry and cell biology and biophysics." Advisor: Leonard D. Dobens. Typescript. Vita. Title from "catalog record" of the print edition Description based on contents viewed May 23, 2008. Includes bibliographical references (leaves 109-115). Online version of the print edition.

Thesis (Ph. D.)--Montana State University--Bozeman, 2005. / Typescript. Chairperson, Graduate Committee: Frances Lefcort. Includes bibliographical references (leaves 96-106).

Thesis (M.S.)--Worcester Polytechnic Institute. / Keywords: minimization, derivatives, correlation, cell migration. Includes bibliographical references (p.52-53).

During C. elegans embryogenesis, myoblasts initially form two rows along the left and right lateral midlines and at ~290 min of development migrate dorsally and ventrally to form the four muscle quadrants present upon hatching (Sulston et al, 1983). As the myoblasts migrate they are still dividing, as are many other cells in their immediate environment. This means the cell-cell contact of cells during migration is dynamic and can vary from animal to animal (Schnabel et al, 1997). This situation creates an environment where the extracellular matrix (ECM) and cell surface contacts are in constant flux, which begs the questions as to how these cells navigate unerringly to their final destination. In an attempt to identify genes mediating these migrations, I performed an RNAi based screen targeting 776 genes predicted to be members of the extracellular matrix (ECM), or one of its receptors. Using both feeding and injection based RNAi, I was able to identify three genes of interest. Knockdowns of F56B3.2 resulted in paralyzed animals with detached muscle, making it a good candidate for a new component of the muscle attachment complex. F33G12.4 knockdowns resulted in an embryonic arrest phenotype with an abnormal muscle lineage, possibly stemming from polarity defects. The only knockdown that resulted in muscle migration defects was that for lam-2, which encodes for the laminin gamma subunit. Analysis of the lam-2 knockdown, as well as knockdowns for the other laminin subunits, revealed dorsal/ventral migration defects as well as a posterior displacement of the anterior-most ventral muscle cells. Investigation of this posterior displacement has led to the identification of a previously un-described anterior muscle migration event and its dependency upon the extension of muscle processes from the leading cells. / Medicine, Faculty of / Medical Genetics, Department of / Graduate

No description available.

No description available.

Chlamydia trachomatis infection targets the mucosal epithelium, where squamous and columnar epithelia can be found. Research on Chlamydia trachomatis-epithelia interaction has predominantly focused on columnar epithelia, with very little known on how Chlamydia trachomatis interacts with the squamous epithelium. The stratification and differentiation processes found in the squamous epithelium might influence chlamydial growth and infection dissemination. For this reason, 3D stratified squamous epithelial cultures were adapted to mimic the stratified squamous epithelium, and chlamydial infection was characterized. Chlamydia trachomatis infection in monolayers and 3D cultures were monitored by immunofluorescence and transmission electron microscopy to characterize inclusion growth and chlamydial interconversion between elementary and reticulate body. We observed that the stratified epithelium varied in susceptibility to Chlamydia trachomatis infection. The undifferentiated basal cells were susceptible to infection, while the terminally differentiated upper layers were resistant. If given access to the basal layer Chlamydia trachomatis is able to disseminate and disrupt the epithelial. This disruption have clinical relevance, such as facilitating secondary infection by other STIs. The use of a punch biopsy in 3D cultures revealed that infected samples were unable to close the wound as efficiently as the mock-infected sample. A simplified 2D wound healing assay confirmed these observations. Additionally, this correlated with a reorganization of hemidesmosomes in Chlamydia trachomatis-infected cells but, most importantly, in bystander uninfected cells within the infected sample. The lack of motility and the hemidesmosomes reorganization was shown to be dependent on myosin II contractility and the chlamydial protein CTL0480. This chlamydial protein recruits MYPT1 to the inclusion membrane, which could potentially prevent the cell from controlling the actomyosin tension. In summary, this is the first study to use a 3D stratified epithelial to determine how Chlamydia interacts with this physiologically relevant tissue. Most importantly, this work demonstrates that Chlamydia trachomatis is able to alter the organization of hemidesmosomes which has never been reported for any other bacterial pathogen.