Stress‐induced phenocopy of <i>C. elegans</i> defines functional steps of sensory organ differentiation

Chow, King Lau; Chan, Kwok Wai

doi:10.1046/j.1440-169x.1999.00459.x

Cited by 11 publications

(8 citation statements)

References 22 publications

(19 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Temporal expression of ram‐5 , as revealed by the GFP reporter E1–GFP in the structural cells, peaks at the beginning of retraction, but is absent earlier when ray cell identity or cell fate are determined. Its expression window is consistent with that defined by heat shock phenocopy and temperature‐sensitive allele analysis on ram gene function (Baird and Emmons, 1990; Chow and Chan, 1999). Expression of ram‐5 declines substantially after the proper ray association is established.…”

Section: Discussionsupporting

confidence: 78%

Expression ofram-5in the structural cell is required for sensory ray morphogenesis inCaenorhabditis elegansmale tail

Nguyen

Hall

et al. 2000

The EMBO Journal

View full text Add to dashboard Cite

Tissue morphogenesis requires complex cellular interaction and communication. The sensory ray in the Caenorhabditis elegans male tail has a simple cellular make-up and a non-essential function, thus providing an ideal model for studying the mechanisms guiding morphogenesis. We present here the analysis of a novel gene, ram-5, mutations of which are characterized by abnormal lumpy rays in the male tail. Microscopic analysis and behavioral studies revealed that lumpy rays contain operational sensory neurons. However, abnormalities were observed in the hypodermis and structural cells as well as in appositions between these two cell types. Molecular cloning and expression studies revealed that the ram-5 gene encodes a transmembrane protein localized in sensory ray support cells, the structural cells. Expression of ram-5 in these cells is required for normal ray morphogenesis. ram-5-dependent cell-cell communication is implicated in organizing the structural cell and the hypodermis, potentially through adhesion at the structural cell-hypodermal cell border.

show abstract

Section: Discussionsupporting

confidence: 78%

Expression ofram-5in the structural cell is required for sensory ray morphogenesis inCaenorhabditis elegansmale tail

Nguyen

Hall

et al. 2000

The EMBO Journal

View full text Add to dashboard Cite

show abstract

“…This defined window has passed the ray cell identity determination step and occurred at 30–36 h post‐L1 arrest. It matches the window defined for ram gene function as revealed by ts alleles of ram genes ( Baird & Emmons 1990) and stress‐induced phenocopy ( Chow & Chan 1999).…”

Section: Resultssupporting

confidence: 62%

Mutations with sensory ray defect unmask cuticular glycoprotein antigens in Caenorhabditis elegans male tail

Chow

2000

Dev Growth Differ

View full text Add to dashboard Cite

Caenorhabditis elegans male tail has nine pairs of bilaterally symmetric ray processes extended into a cuticular fan. The formation of these structures involves both cell lineage differentiation and cellular morphogenesis. Nine mutations were examined, all of which presented an amorphous ray phenotype. Glycoconjugates carrying an N-acetylglucosamine (GlcNAc) epitope were detected at a high level in their male bursa. It was shown that these antigens are not responsible for the morphological defects. It was further demonstrated that these ram and mab gene products represent critical components for male tail cuticle organization. Mutations of them abolish the integrity of the male bursal cuticle and unmask the underlying GlcNAc epitope.

show abstract

“…Thermotolerance is a well-known phenomenon associated with synthesis of HSPs at moderate temperatures that allow the cell and the whole organism to tolerate subsequent, higher stress conditions (15,16,28,29,33). Different types of embryological defects have been described in other organisms depending on the exact timing of the stress (6,10,31). All of these defects induced by heat can be prevented by inducing thermotolerance (31).…”

Section: Discussionmentioning

confidence: 99%

Changes in Membrane Fluid State and Heat Shock Response Cause Attenuation of Virulence

et al. 2010

View full text Add to dashboard Cite

So far attenuation of pathogens has been mainly obtained by chemical or heat treatment of microbial pathogens. Recently, live attenuated strains have been produced by genetic modification. We have previously demonstrated that in several prokaryotes as well as in yeasts and mammalian cells the heat shock response is controlled by the membrane physical state (MPS). We have also shown that in Salmonella enterica serovar Typhimurium LT2 (Salmonella Typhimurium) overexpression of a ⌬ 12 -desaturase gene alters the MPS, inducing a sharp impairment of transcription of major heat shock genes and failure of the pathogen to grow inside macrophage (M⌽) (A. Porta et al., J. Bacteriol. 192:1988Bacteriol. 192: -1998Bacteriol. 192: , 2010). Here, we show that overexpression of a homologous ⌬ 9 -desaturase sequence in the highly virulent G217B strain of the human fungal pathogen Histoplasma capsulatum causes loss of its ability to survive and persist within murine M⌽ along with the impairment of the heat shock response. When the attenuated strain of H. capsulatum was injected in a mouse model of infection, it did not cause disease. Further, treated mice were protected when challenged with the virulent fungal parental strain. Attenuation of virulence in M⌽ of two evolutionarily distant pathogens was obtained by genetic modification of the MPS, suggesting that this is a new method that may be used to produce attenuation or loss of virulence in both other intracellular prokaryotic and eukaryotic pathogens. This new procedure to generate attenuated forms of pathogens may be used eventually to produce a novel class of vaccines based on the genetic manipulation of a pathogen's membrane fluid state and stress response.So far, a methodology to obtain live attenuated strains has not been generated for fungal pathogens. With respect to parasites, a live attenuated strain of Toxoplasma has been produced. However, this modified strain was used to develop a vaccine that was considered expensive, caused side effects, and had a short shelf life. Furthermore, the authors emphasized that this vaccine might revert to a pathogenic strain and, therefore, was not considered suitable for human use (17). In Leishmania and other parasites, as yet none of the current candidate subunit vaccines has achieved complete protection reproducibly. Attempts to develop an effective vaccine to control leishmaniasis have been shown to be feasible, but no vaccine is in active clinical use (18). The ability to create genetically modified pathogens by eliminating virulence or essential genes is considered a powerful alternative in the development of an effective protective vaccine. The current genetic procedures are based on the use of specific (virulence) genes that may cause attenuation and are species specific. In other words, a given method of attenuation may be effective in a specific organism but not in other pathogens.We have previously shown in several prokaryotic and eukaryotic cells, including pathogens such as Salmonella (34) and in the human pathogenic fu...

show abstract

Stress‐induced phenocopy of C. elegans defines functional steps of sensory organ differentiation

Cited by 11 publications

References 22 publications

Expression ofram-5in the structural cell is required for sensory ray morphogenesis inCaenorhabditis elegansmale tail

Expression ofram-5in the structural cell is required for sensory ray morphogenesis inCaenorhabditis elegansmale tail

Mutations with sensory ray defect unmask cuticular glycoprotein antigens in Caenorhabditis elegans male tail

Changes in Membrane Fluid State and Heat Shock Response Cause Attenuation of Virulence

Contact Info

Product

Resources

About