Abstract
Prolonged exposure to stress and the resulting over-stimulation of the HPA system are often detrimental to the homeostasis of an organism. In fact, chronic stress is believed to affect the pathology of several disease states including coronary heart disease and hypertension, diabetes and obesity. In humans, mutations in the GLC1A gene have been associated with primary open angle glaucoma. Previous studies on this gene have suggested that its expression is also affected by the same factors that mediate the stress response. With the ultimate goal of using the nematode, Caenorhabditis elegans, as an invertebrate model for glaucoma, we have measured the stress responsiveness of the cof-2 gene, one of two C. elegans proteins with significant homology to the myocilin olfactomedin domain. We show that both cof-2 mRNA and protein expression are developmentally regulated and that both are affected by heat shock stress.
Publication types
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Research Support, U.S. Gov't, Non-P.H.S.
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Caenorhabditis elegans / genetics
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Caenorhabditis elegans / growth & development
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Caenorhabditis elegans / metabolism*
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Caenorhabditis elegans Proteins / genetics
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Caenorhabditis elegans Proteins / metabolism*
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Disease Models, Animal
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Extracellular Matrix Proteins / metabolism
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Gene Expression
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Gene Expression Regulation, Developmental*
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Glaucoma / genetics
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Glaucoma / metabolism*
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Glycoproteins / metabolism
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HSP90 Heat-Shock Proteins / genetics
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HSP90 Heat-Shock Proteins / metabolism
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Heat-Shock Response / genetics
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Heat-Shock Response / physiology
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Membrane Proteins / genetics
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Membrane Proteins / metabolism*
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RNA, Messenger / genetics
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RNA, Messenger / metabolism
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Stress, Physiological / genetics
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Stress, Physiological / metabolism*
Substances
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COF-2 protein, C elegans
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Caenorhabditis elegans Proteins
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Extracellular Matrix Proteins
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Glycoproteins
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HSP90 Heat-Shock Proteins
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Membrane Proteins
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RNA, Messenger
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olfactomedin