Increased production of genetic mosaics in Habrobracon juglandis by cold shock of newly oviposited eggs

Development ◽  
1976 ◽  
Vol 36 (1) ◽  
pp. 127-131
Author(s):  
R. M. Petters ◽  
D. S. Grosch
Keyword(s):  
Heat Shock ◽  
Cold Shock ◽  
Differential Mortality ◽  
Wild Type ◽  
Cleavage Stage ◽  
Genetic Mosaics

Eggs from an ebony stock exposed to 5·5°C prior to syngamy exhibited increased production of genetic mosaics in comparison with untreated eggs from the same females. No increase in mosaic production occurred for cold-shocked cleavage-stage embryos from the ebony stock or from pre-cleavage cold-shocked eggs from a wild-type stock. Heat shock of pre-syngamy eggs also failed to increase the production of genetic mosaics. These findings are onsistent with predictions based on the post-cleavage fertilization theory of mosaic origin in Habrobracon or with a hypothesis of differential mortality.

scholarly journals Impaired Temperature Stress Response of a Streptococcus thermophilus deoD Mutant

2003 ◽  
Vol 69 (2) ◽  
pp. 1287-1289 ◽  
Author(s):  
Mario Varcamonti ◽  
Maria R. Graziano ◽  
Romilde Pezzopane ◽  
Gino Naclerio ◽  
Slavica Arsenijevic ◽  
...  
Keyword(s):  
Growth Rate ◽  
Stress Response ◽  
Heat Shock ◽  
Temperature Stress ◽  
Streptococcus Thermophilus ◽  
Wild Type ◽  
Temperature Shock ◽  
Dual Response ◽  
Survival Capacity

ABSTRACT An insertional deoD mutant of Streptococcus thermophilus strain SFi39 had a reduced growth rate at 20°C and an enhanced survival capacity to heat shock compared to the wild type, indicating that the deoD product is involved in temperature shock adaptation. We report evidence that ppGpp is implicated in this dual response.

Role of heat shock transcription factor in yeast metallothionein gene expression

1991 ◽  
Vol 11 (7) ◽  
pp. 3676-3681
Author(s):  
W M Yang ◽  
W Gahl ◽  
D Hamer
Keyword(s):  
Gene Expression ◽  
Transcription Factor ◽  
Heat Shock ◽  
Gene Transcription ◽  
Heat Shock Factor ◽  
Heat Shock Transcription Factor ◽  
Wild Type ◽  
Promoter Sequences ◽  
Metallothionein Gene ◽  
Upstream Promoter

The induction of Saccharomyces cerevisiae metallothionein gene transcription by Cu and Ag is mediated by the ACE1 transcription factor. In an effort to detect additional stimuli and factors that regulate metallothionein gene transcription, we isolated a Cu-resistant suppressor mutant of an ACE1 deletion strain. Even in the absence of metals, the suppressor mutant exhibited high basal levels of metallothionein gene transcription that required upstream promoter sequences. The suppressor gene was cloned, and its predicted product was shown to correspond to yeast heat shock transcription factor with a single-amino-acid substitution in the DNA-binding domain. The mutant heat shock factor bound strongly to metallothionein gene upstream promoter sequences, whereas wild-type heat shock factor interacted weakly with the same region. Heat treatment led to a slight but reproducible induction of metallothionein gene expression in both wild-type and suppressor strains, and Cd induced transcription in the mutant strain. These studies provide evidence for multiple pathways of metallothionein gene transcriptional regulation in S. cerevisiae.

Cell-autonomous shift from axial to paraxial mesodermal development in zebrafish floating head mutants

Development ◽  
1995 ◽  
Vol 121 (12) ◽  
pp. 4257-4264 ◽  
Author(s):  
M.E. Halpern ◽  
C. Thisse ◽  
R.K. Ho ◽  
B. Thisse ◽  
B. Riggleman ◽  
...  
Keyword(s):  
Neural Tube ◽  
Single Cells ◽  
Floor Plate ◽  
Paraxial Mesoderm ◽  
Wild Type ◽  
Genetic Mosaics ◽  
Essential Step ◽  
Ventral Neural Tube ◽  
Mesodermal Development

Zebrafish floating head mutant embryos lack notochord and develop somitic muscle in its place. This may result from incorrect specification of the notochord domain at gastrulation, or from respecification of notochord progenitors to form muscle. In genetic mosaics, floating head acts cell autonomously. Transplanted wild-type cells differentiate into notochord in mutant hosts; however, cells from floating head mutant donors produce muscle rather than notochord in wild-type hosts. Consistent with respecification, markers of axial mesoderm are initially expressed in floating head mutant gastrulas, but expression does not persist. Axial cells also inappropriately express markers of paraxial mesoderm. Thus, single cells in the mutant midline transiently co-express genes that are normally specific to either axial or paraxial mesoderm. Since floating head mutants produce some floor plate in the ventral neural tube, midline mesoderm may also retain early signaling capabilities. Our results suggest that wild-type floating head provides an essential step in maintaining, rather than initiating, development of notochord-forming axial mesoderm.

scholarly journals HrcA and DnaK are important for static and continuous-flow biofilm formation and disinfectant resistance in Listeria monocytogenes

Microbiology ◽  
2010 ◽  
Vol 156 (12) ◽  
pp. 3782-3790 ◽  
Author(s):  
Stijn van der Veen ◽  
Tjakko Abee
Keyword(s):  
Listeria Monocytogenes ◽  
Heat Shock ◽  
Heat Shock Response ◽  
Peracetic Acid ◽  
Continuous Flow ◽  
Biofilm Formation ◽  
Benzalkonium Chloride ◽  
Wild Type ◽  
Shock Response ◽  
Disinfectant Resistance

The food-borne pathogen Listeria monocytogenes is able to form biofilms in food processing environments. Since biofilms are generally difficult to eradicate during clean-up procedures, they pose a major risk for the food industry. Stress resistance mechanisms involved in L. monocytogenes biofilm formation and disinfectant resistance have, to our knowledge, not been identified thus far. In this study, we investigated the role of hrcA, which encodes the transcriptional regulator of the class I heat-shock response, and dnaK, which encodes a class I heat-shock response chaperone protein, in static and continuous-flow biofilm formation and resistance against benzalkonium chloride and peracetic acid. Induction of both hrcA and dnaK during continuous-flow biofilm formation was observed using quantitative real-time PCR and promoter reporters. Furthermore, in-frame deletion and complementation mutants of hrcA and dnaK revealed that HrcA and DnaK are required to reach wild-type levels of both static and continuous-flow biofilms. Finally, disinfection treatments of planktonic-grown cells and suspended static and continuous-flow biofilm cells of wild-type and mutants showed that HrcA and DnaK are important for resistance against benzalkonium chloride and peracetic acid. In conclusion, our study revealed that HrcA and DnaK are important for L. monocytogenes biofilm formation and disinfectant resistance.

scholarly journals Cold Shock Proteins of Lactococcus lactis MG1363 Are Involved in Cryoprotection and in the Production of Cold-Induced Proteins

2001 ◽  
Vol 67 (11) ◽  
pp. 5171-5178 ◽  
Author(s):  
Jeroen A. Wouters ◽  
Hélène Frenkiel ◽  
Willem M. de Vos ◽  
Oscar P. Kuipers ◽  
Tjakko Abee
Keyword(s):  
Low Temperature ◽  
Lactococcus Lactis ◽  
Type Strain ◽  
Wild Type Strain ◽  
Cold Shock ◽  
Transcriptional Level ◽  
Wild Type ◽  
Cold Shock Proteins ◽  
Shock Proteins ◽  
Induced Proteins

ABSTRACT Members of the group of 7-kDa cold-shock proteins (CSPs) are the proteins with the highest level of induction upon cold shock in the lactic acid bacterium Lactococcus lactis MG1363. By using double-crossover recombination, two L. lactis strains were generated in which genes encoding CSPs are disrupted: L. lactis NZ9000ΔAB lacks the tandemly orientatedcspA and cspB genes, and NZ9000ΔABE lackscspA, cspB, and cspE. Both strains showed no differences in growth at normal and at low temperatures compared to that of the wild-type strain, L. lactis NZ9000. Two-dimensional gel electrophoresis showed that upon disruption of thecspAB genes, the production of remaining CspE at low temperature increased, and upon disruption of cspA, cspB, and cspE, the production of CspD at normal growth temperatures increased. Northern blot analysis showed that control is most likely at the transcriptional level. Furthermore, it was established by a proteomics approach that some (non-7-kDa) cold-induced proteins (CIPs) are not cold induced in the csp-lacking strains, among others the histon-like protein HslA and the signal transduction protein LlrC. This supports earlier observations (J. A. Wouters, M. Mailhes, F. M. Rombouts, W. M. De Vos, O. P. Kuipers, and T. Abee, Appl. Environ. Microbiol. 66:3756–3763, 2000). that the CSPs of L. lactis might be directly involved in the production of some CIPs upon low-temperature exposure. Remarkably, the adaptive response to freezing by prior exposure to 10°C was significantly reduced in strain NZ9000ΔABE but not in strain NZ9000ΔAB compared to results with wild-type strain NZ9000, indicating a notable involvement of CspE in cryoprotection.

Transcriptional activation and subsequent control of the human heat shock gene during adenovirus infection

1983 ◽  
Vol 3 (11) ◽  
pp. 2058-2065 ◽  
Author(s):  
H T Kao ◽  
J R Nevins
Keyword(s):  
Heat Shock ◽  
Transcriptional Activation ◽  
Peak Level ◽  
Heat Shock Gene ◽  
Adenovirus Infection ◽  
Wild Type ◽  
Rapid Turnover ◽  
Transformed Cell Line ◽  
Shock Gene ◽  
E1a Gene

A cDNA copy of the major human heat shock mRNA was cloned. The clone is complementary to the mRNA encoding the major 70-kilodalton heat shock protein as shown by hybrid arrest translation. We utilized the cloned DNA to measure induction of the gene during adenovirus infection. The mRNA increases in abundance approximately 100-fold during a wild-type adenovirus infection but does not increase more than 2-fold during an infection in which there is no E1A gene function [high multiplicity of infection of an E1A (-) mutant]. Furthermore, by measuring transcription in isolated nuclei, we found that the induction was transcriptional and was mediated by the E1A gene product. The induction was not maintained, however. After a peak level was obtained, transcription returned to preinfection levels. This decline was also reflected in the cytoplasmic mRNA abundance indicating a rapid turnover of the heat shock mRNA. This rapid turnover of the heat shock mRNA appears to be induced by the viral infection since the heat shock mRNA was found to be stable when synthesized in an adenovirus-transformed cell line.

Ubiquitin gene expression in Dictyostelium is induced by heat and cold shock, cadmium, and inhibitors of protein synthesis

1988 ◽  
Vol 90 (1) ◽  
pp. 51-58 ◽  
Author(s):  
A. Muller-Taubenberger ◽  
J. Hagmann ◽  
A. Noegel ◽  
G. Gerisch
Keyword(s):  
Gene Expression ◽  
Protein Synthesis ◽  
Heat Shock ◽  
Differential Expression ◽  
Dictyostelium Discoideum ◽  
Heat Shock Response ◽  
Cold Shock ◽  
Multifunctional Protein ◽  
Cadmium Treatment ◽  
Shock Response

Ubiquitin is a highly conserved, multifunctional protein, which is implicated in the heat-shock response of eukaryotes. The differential expression of the multiple ubiquitin genes in Dictyostelium discoideum was investigated under various stress conditions. Growing D. discoideum cells express four major ubiquitin transcripts of sizes varying from 0.6 to 1.9 kb. Upon heat shock three additional ubiquitin mRNAs of 0.9, 1.2 and 1.4 kb accumulate within 30 min. The same three transcripts are expressed in response to cold shock or cadmium treatment. Inhibition of protein synthesis by cycloheximide leads to a particularly strong accumulation of the larger ubiquitin transcripts, which code for polyubiquitins. Possible mechanisms regulating the expression of ubiquitin transcripts upon heat shock and other stresses are discussed.

The terminal differentiation factor LIN-29 is required for proper vulval morphogenesis and egg laying in Caenorhabditis elegans

Development ◽  
1997 ◽  
Vol 124 (21) ◽  
pp. 4333-4342 ◽  
Author(s):  
J.C. Bettinger ◽  
S. Euling ◽  
A.E. Rougvie
Keyword(s):  
Caenorhabditis Elegans ◽  
Terminal Differentiation ◽  
Egg Laying ◽  
Small Subset ◽  
Wild Type ◽  
Vulval Development ◽  
Genetic Mosaics ◽  
Hypodermal Cell ◽  
Heterochronic Gene ◽  
Final Molt

Caenorhabditis elegans vulval development culminates during exit from the L4-to-adult molt with the formation of an opening through the adult hypodermis and cuticle that is used for egg laying and mating. Vulva formation requires the heterochronic gene lin-29, which triggers hypodermal cell terminal differentiation during the final molt. lin-29 mutants are unable to lay eggs or mate because no vulval opening forms; instead, a protrusion forms at the site of the vulva. We demonstrate through analysis of genetic mosaics that lin-29 is absolutely required in a small subset of lateral hypodermal seam cells, adjacent to the vulva, for wild-type vulva formation and egg laying. However, lin-29 function is not strictly limited to the lateral hypodermis. First, LIN-29 accumulates in many non-hypodermal cells with known roles in vulva formation or egg laying. Second, animals homozygous for one lin-29 allele, ga94, have the vulval defect and cannot lay eggs, despite having a terminally differentiated adult lateral hypodermis. Finally, vulval morphogenesis and egg laying requires lin-29 activity within the EMS lineage, a lineage that does not generate hypodermal cells.

Analysis of the function of the 70-kilodalton cyclase-associated protein (CAP) by using mutants of yeast adenylyl cyclase defective in CAP binding

1993 ◽  
Vol 13 (7) ◽  
pp. 4087-4097
Author(s):  
J Wang ◽  
N Suzuki ◽  
Y Nishida ◽  
T Kataoka
Keyword(s):  
Heat Shock ◽  
Adenylyl Cyclase ◽  
Gene Replacement ◽  
Yeast Cells ◽  
Cyclase Activity ◽  
In Vitro Mutagenesis ◽  
Wild Type ◽  
Adenylyl Cyclase Activity

In Saccharomyces cerevisiae, adenylyl cyclase forms a complex with the 70-kDa cyclase-associated protein (CAP). By in vitro mutagenesis, we assigned a CAP-binding site of adenylyl cyclase to a small segment near its C terminus and created mutants which lost the ability to bind CAP. CAP binding was assessed first by observing the ability of the overproduced C-terminal 150 residues of adenylyl cyclase to sequester CAP, thereby suppressing the heat shock sensitivity of yeast cells bearing the activated RAS2 gene (RAS2Val-19), and then by immunoprecipitability of adenylyl cyclase activity with anti-CAP antibody and by direct measurement of the amount of CAP bound. Yeast cells whose chromosomal adenylyl cyclase genes were replaced by the CAP-nonbinding mutants possessed adenylyl cyclase activity fully responsive to RAS2 protein in vitro. However, they did not exhibit sensitivity to heat shock in the RAS2Val-19 background. When glucose-induced accumulation of cyclic AMP (cAMP) was measured in these mutants carrying RAS2Val-19, a rapid transient rise indistinguishable from that of wild-type cells was observed and a high peak level and following persistent elevation of the cAMP concentration characteristic of RAS2Val-19 were abolished. In contrast, in the wild-type RAS2 background, similar cyclase gene replacement did not affect the glucose-induced cAMP response. These results suggest that the association with CAP, although not involved in the in vivo response to the wild-type RAS2 protein, is somehow required for the exaggerated response of adenylyl cyclase to activated RAS2.

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