A neomorphic allele of klp-11 causes abnormal body morphology in C. elegans
Date Issued
2014
Date
2014
Author(s)
Chen, Yi-Yin
Abstract
Morphogenesis is an essential process for a multi-cellular organism to develop into its characteristic body shape. In C. elegans, this process is largely controlled by the development of hypodermis and muscle tissues. In a genetic screen, we isolated the klp-11(tp8) mutant with an abnormal body shape, which has an arcuate swell in the body surface, referred as “bulge” here. klp-11 encodes a type II kinesin motor protein subunit. tp8 caused an amino acid substitution from glycine to aspartate in a highly conserved residue in the motor domain. Deletion of klp-11 by RNA interference caused no effect in the wild-type but suppressed the bulge phenotype in the klp-11(tp8) mutant, suggesting that tp8 may be a neomorphic allele of klp-11. We found that cells in the bulge consists of hypodermal, muscle cells or neurons using cell-specific fluorescence reporters. Consistently, klp-11 was found to be expressed in these cells. It is possible that tp8 may elicit an abnormal function of a kinesin complex to cause bulge formation from these cells. We next examined the ultrastructural defects in the bulge and other part(s) of the klp-11(tp8) mutant, using the transmission electron microscopy (TEM), and find muscle cells and neurons here within the bulge region, consistent with the fluorescent microscopy result. We also found the hypodermal cells grow under the muscle cells in the klp-11(tp8) mutant. These data show that tp8 causes multiple defects in various cell types. We observed many vesicles, neurons, muscle and hypodermal cells accumulated in the bulge region, so we hypothesized that the bulge may be caused by mis-regulation of vesicle transport and/or cell proliferation. We expressed wild-type klp-11 under the control of muscle-specific promoter could partially rescue the bulge phenotype indicated that klp-11 may function at least in muscle cells to prevent the bulge formation. In addition, because KLP-11 forms a heterotrimer with KLP-20 and KAP-1 and function as intraflagellar transport (IFT) in ciliated sensory neurons, we speculate that klp-11(tp8) may influence cargo transport by abnormal cargo accumulation in the minus end or absence of cargo in the plus end to cause bulge phenotype.
Subjects
型態異常
驅動蛋白
Type
thesis
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