In this thesis we developed a new mechanics model of the primary cilium and analyzed its bending behavior. The primary cilium that extends from the cell surface can detect the mechanical signals of the surrounding environment. Moreover, through its deflection and bending angle, the primary cilium can communicate with the cell regarding the extracellular. Scientists have shown that dysfunction of primary cilia can lead to many diseases as cilia are believed to play an important role in transmitting signals in cells. A good model of primary cilium can aid in the understanding of the mechanism of its bending movement. Furthermore, a good model is important for determining how the primary cilium contributes to convert mechanical signals into biochemical ones. Previous models have ignored the basal body and transition fiber that are located at the base of the primary cilium. However, it is clear that the elastic basal body and transition fibers should have a significant effect on the deformation of the whole structure. Aiming to address this issue, we established a model with a rotational spring representing the confinement induced by the basal body and transition fibers. Specially, we developed two governing equations for two different conditions, namely uniformly distributed load and spatially varying load. In addition, this model is valid for situations where the deflection is large. To obtain the results the shooting and Newton-Raphson methods are used to solve the governing equations numerically. Then, we compared the numerical results with experimental data to test the validity of the model. Comparison between our model predictions and experimental data showed that the governing equation for spatially varying load described the bending behavior of the primary cilium very well under various realistic conditions, including cases where the flow field is not uniform both spatially and temporally fluid flow with variable velocity. / published_or_final_version / Mechanical Engineering / Master / Master of Philosophy

Thesis supervisor: Charles Yeaman. Includes bibliographic references (p. 94-100).

Thesis (Ph. D.)--University of Wisconsin--Madison, 1981. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references.

Thesis--University of Wisconsin--Madison. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 152-161).

Thesis (M.S.)--University of Wisconsin--Madison. / Typescript. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 44-47).

The object of this study is to understand the effect of food on the speed of ciliary movement of the gill of cultured hard clam. It is known that the speed of ciliary movement of the gill of cultured hard clam is affected by temperature and salinity, so this study explores the influence of food on speed of ciliary movement of the gill under the different temperature-salinity conditions. This study used three methods to test for the speed of ciliary movement of the gill of cultured hard clam. By the first method, using a piece of aluminum foil tested for the gill in vivo, demonstrated none of Isochysis galbana¡BSynechococcus sp.¡Btemperature¡Bphase and sizes of aluminum foil affected significantly on the speed of ciliary movement of the gill of cultured hard clam. By the second method, using sand tested for the gill in vitro, demonstrated adding I. galbana or the high concentration (1¡Ñ105 cells ml-1) of Tetraselmis chui caused the speed of ciliary movement of the gill of cultured hard clam increased significantly at room temperature, 15 psu. At 32¢J, only the low concentration(1¡Ñ103 cells ml-1) of I. galbana affected significantly the speed of ciliary movement of the gill, and the mean speed of 1.36 cm/min at 32¢J was slower than the mean speed of 2.05 cm/min at room temperature. At 10 psu, both high and low concentration of I. galbana influenced the speed of ciliary movement of the gill, besides the mean speed of 2.82 cm/min at 10 psu was faster than the mean speed at 25 psu. The ciliary movement of the gill of cultured hard clam had no response to I. galbana, and the mean speed of 1.76 cm/min at 25 psu. By the third method, using sands tested for the gill in vivo, the results showed that adding the high concentration of I. galbana caused the speed of ciliary movement of the gill of cultured hard clam to increase significantly, and 33.85¢H of the change of this speed was not different significantly with 33.00¢H of the change of the speed of the gill in vitro adding the high of I. galbana. Besides, the mean speed of 1.99 cm/min by using sands tested for the gill in vivo was not also different significantly with the mean speed of the gill in vitro.Based on the above results, the result tested the gill in vitro by the second method was similar to the result tested the gill in vivo by the third method. Under the same condition, the maximum change of speed of ciliary movement of the gill was about sixty percent from the experiment of adding the low concentration of I. galbana, and the minimum change of speed was about ten percent from the experiment of the low concentration of T. chui. The change of the speed of ciliary movement of the gill of cultured hard clam was most affected by I. galbana, and the change was about thirty percent.

Thesis (M.S.)--Rochester Institute of Technology, 2009. / Typescript. Includes bibliographical references (leaves 132-134).

No description available.

Drosophila provide an excellent model organism in which to study cilia as there are only two ciliated cell types; the sensory neurons and sperm cells. The chordotonal neuron is one such ciliated cell and is required for hearing, proprioception and gravitaxis. Mechanical manipulation of the cilium that extends from the neuronal dendrite is required for signal transduction. Chordotonal neuronal differentiation is regulated by a transcription factor cascade. Atonal begins the cascade, which is then continued by RFX and Fd3F for ciliary genes (Cachero et al 2011, Newton et al 2012). Genes expressed in developing chordotonal neurons are downstream of these transcription factors and their characterisation can further elucidate how neuronal differentiation is regulated. Ciliary genes are highly enriched in developing chordotonal cells; uncharacterised genes enriched in these cells can therefore be considered candidate ciliary genes (Cachero et al 2011). A behavioural assay was conducted to identify further genes that could have a role in ciliary formation and function. Candidate genes were identified by combining enrichment data with previous genomic, proteomic and transcriptomic studies of cilia. A climbing assay of RNAi mediated knock down of these genes identified a number of candidates for future work. One gene found to be highly enriched in developing chordotonal neurons is CG11253. CG11253EY10866 P element insertion mutant flies show a mild uncoordinated phenotype in a climbing assay consistent with reduced chordotonal organ function. Male flies are also infertile due to a lack of motile sperm. CG11253 is expressed in motile ciliated cells and is conserved in organisms with motile cilia. CG11253 expression is also regulated by RFX and Fd3F, suggesting that it is involved in cilium motility. This was confirmed by electron microscopy, which showed disruption of axonemal dynein arm localisation in chordotonal cilia and sperm flagella. A CG11253::mVenus fusion protein was found to localise mainly to the cytoplasm and to a lesser extent the cilia of chordotonal neurons. Patients with symptoms consistent with Primary Ciliary Dyskinesia (PCD), a condition caused by cilium immotility, have subsequently been found to have point mutations in ZMYND10, the human homologue of CG11253. The identification of PCD patients with ZMYND10 mutations showed that investigating cilium motility in Drosophila chordotonal neurons could identify novel PCD genes. It was thought that investigating previously uncharacterised targets of Fd3F could identify novel genes involved in cilium motility and thus candidate PCD genes. CG31320 is a gene regulated by RFX and Fd3F and conserved in organisms with motile cilia. RNAi mediated knock down of CG31320 resulted in both a mild uncoordinated phenotype and male infertility due to a lack of motile sperm. Electron microscopy showed a complete loss of axonemal dynein arms in chordotonal neuron cilia. An mVenus fusion protein of CG6971, an inner dynein arm component, was also mislocalised from the cilia in CG3132027 deletion mutant larvae. This shows that CG31320 is required for the appropriate localisation of the axonemal dynein arms and thus cilium motility. This further showed that uncharacterised genes enriched in chordotonal neurons and regulated by Fd3F could be novel ciliary genes required for cilium motility. Our collaborators and Horani et al (2012) showed that the human homologue of CG31320 (HEATR2) is mutated in patients with PCD, further confirming that this method can be used to identify PCD genes. I have identified two factors required for cilium motility. Disruption of the axonemal dynein arms in both cases results in reduced coordination, and lack of fertility due to sperm immotility. Mutations in the human homologues of these genes have been found to result in PCD. This indicates that further PCD genes could be identified from genes enriched in Drosophila chordotonal neurons that are regulated by Fd3F.

No description available.