8 resultados para Environmental Stress Cracking (esc)
em Consorci de Serveis Universitaris de Catalunya (CSUC), Spain
Resumo:
Yeast successfully adapts to an environmental stress by altering physiology and fine-tuning metabolism. This fine-tuning is achieved through regulation of both gene expression and protein activity, and it is shaped by various physiological requirements. Such requirements impose a sustained evolutionary pressure that ultimately selects a specific gene expression profile, generating a suitable adaptive response to each environmental change. Although some of the requirements are stress specific, it is likely that others are common to various situations. We hypothesize that an evolutionary pressure for minimizing biosynthetic costs might have left signatures in the physicochemical properties of proteins whose gene expression is fine-tuned during adaptive responses. To test this hypothesis we analyze existing yeast transcriptomic data for such responses and investigate how several properties of proteins correlate to changes in gene expression. Our results reveal signatures that are consistent with a selective pressure for economy in protein synthesis during adaptive response of yeast to various types of stress. These signatures differentiate two groups of adaptive responses with respect to how cells manage expenditure in protein biosynthesis. In one group, significant trends towards downregulation of large proteins and upregulation of small ones are observed. In the other group we find no such trends. These results are consistent with resource limitation being important in the evolution of the first group of stress responses.
Resumo:
Plants, like humans and other animals, also get sick, exhibit disease symptoms, and die. Plant diseases are caused by environmental stress, genetic or physiological disorders and infectious agents including viroids, viruses, bacteria and fungi. Plant pathology originated from the convergence of microbiology, botany and agronomy; its ultimate goal is the control of plant disease. Microbiologists have been attracted to this field of research because of the need for identification of the agents causing infectious diseases in economically important crops. In 1878—only two years after Pasteur and Koch had shown for the first time that anthrax in animals was caused by a bacteria—Burril, in the USA, discovered that the fire blight disease of apple and pear was also caused by a bacterium (nowadays known as Erwinia amylovora). In 1898, Beijerinck concluded that tobacco mosaic was caused by a “contagium vivum fluidum” which he called a virus. In 1971, Diener proved that a potato disease named potato spindle tuber was caused by infectious RNA which he called viroid
Resumo:
Les particularitats de les poblacions amfíbiques que viuen en zones semiàrides sotmeses a un alt estrès ambiental es posen de manifest mitjançant estudis d’esqueletocronologia. L’estudi pretén avaluar la correlació histològica entre les marques de creixement (lines of arrested growth [LAG]) que es visualitzen en les falanges dels dits i l’edat d’individus de gripau corredor (Epidelea calamita). Existeix una correspondència entre el nombre de LAG i el nombre d’hibernacions, de manera que, en un principi, s’entén cada una de les línies com un any de vida de l’individu. En els resultats trobats mitjançant l’anàlisi dels talls de les falanges, s’aprecien un conjunt de línies múltiples que es consideren com una hibernació interrompuda per petits creixements durant els períodes més càlids de l’hivern i en certa part també per les ocasionals precipitacions. Els resultats obtinguts suggereixen l’existència d’un patró de creixement, en les poblacions d’amfibis en zones semiàrides, diferent de qualsevol altre trobat en amfibis de zones temperades.
Resumo:
We have analyzed the heat stress response in the yeast Saccharomyces cerevisiae by determining mRNA levels and transcription rates for the whole transcriptome after a shift from 25uC to 37uC. Using an established mathematical algorithm, theoretical mRNA decay rates have also been calculated from the experimental data. We have verified the mathematical predictions for selected genes by determining their mRNA decay rates at different times during heat stress response using the regulatable tetO promoter. This study indicates that the yeast response to heat shock is not only due to changes in transcription rates, but also to changes in the mRNA stabilities. mRNA stability is affected in 62% of the yeast genes and it is particularly important in shaping the mRNA profile of the genes belonging to the environmental stress response. In most cases, changes in transcription rates and mRNA stabilities are homodirectional for both parameters, although some interesting cases of antagonist behavior are found. The statistical analysis of gene targets and sequence motifs within the clusters of genes with similar behaviors shows that both transcriptional and post-transcriptional regulons apparently contribute to the general heat stress response by means of transcriptional factors and RNA binding proteins.
Resumo:
En aquest projecte es presenta la realització d’un sistema d’assaig de la corrosió sota tensió (stress corrosion cracking, SCC) i un estudi de l’efecte de l’SCC sobre dos acers d’eina per matrius d’estampació en calent. L’SCC és la formació i propagació d’esquerdes en un material degut a la interacció de tres factors: un medi corrosiu, un material susceptible i una tensió estàtica aplicada. Aquestes esquerdes són difícils de detectar i poden provocar fallades catastròfiques inesperades i, en concret, s’ha detectat aquest fenomen en matrius refrigerades d’estampació en calent. Es pretén dissenyar i construir un dispositiu d’assaig SCC per tal d’utilitzar-lo per l’estudi dels materials 1.2367 i 1.2343 en condicions d’aigua de xarxa, aigua destil·lada i inhibidor. Aquests assaigs es realitzen a les temperatures de 40 i 80ºC ja que un estudi previ ha simulat les condicions de temperatura als canals de refrigeració de les matrius d’estampació en calent i s’ha vist que aquestes són les temperatures assolides. La raó d’estudiar aquests materials és perquè són dos acers d’eina per treball en calent convencionals, usats en l’àmbit de les matrius refrigerades d’estampació en calent i en general en processos de conformat en calent (forja, moldeig). S’estudia el comportament a tracció d’aquests materials en aquestes condicions comparant-lo amb el mateix assaig però en condicions en aire, i s’avaluen les diferències en la tensió màxima, la ductilitat, el mecanisme de fractura o l’esquerdament sofert. Es fa un estudi fractogràfic de les mostres mitjançant microscòpia electrònica de rastreig (SEM) i un estudi de les superfícies laterals i del secondary cracking mitjançant microscòpia òptica. Es comparen els diferents resultats obtinguts i es determina en quines condicions s’ha desenvolupat SCC i en quines no, en quina intensitat i quines opcions hi ha per evitar-lo.
Resumo:
Background: Cells have the ability to respond and adapt to environmental changes through activation of stress-activated protein kinases (SAPKs). Although p38 SAPK signalling is known to participate in the regulation of gene expression little is known on the molecular mechanisms used by this SAPK to regulate stress-responsive genes and the overall set of genes regulated by p38 in response to different stimuli.Results: Here, we report a whole genome expression analyses on mouse embryonic fibroblasts (MEFs) treated with three different p38 SAPK activating-stimuli, namely osmostress, the cytokine TNFα and the protein synthesis inhibitor anisomycin. We have found that the activation kinetics of p38α SAPK in response to these insults is different and also leads to a complex gene pattern response specific for a given stress with a restricted set of overlapping genes. In addition, we have analysed the contribution of p38α the major p38 family member present in MEFs, to the overall stress-induced transcriptional response by using both a chemical inhibitor (SB203580) and p38α deficient (p38α-/-) MEFs. We show here that p38 SAPK dependency ranged between 60% and 88% depending on the treatments and that there is a very good overlap between the inhibitor treatment and the ko cells. Furthermore, we have found that the dependency of SAPK varies depending on the time the cells are subjected to osmostress. Conclusions: Our genome-wide transcriptional analyses shows a selective response to specific stimuli and a restricted common response of up to 20% of the stress up-regulated early genes that involves an important set of transcription factors, which might be critical for either cell adaptation or preparation for continuous extra-cellular changes. Interestingly, up to 85% of the up-regulated genes are under the transcriptional control of p38 SAPK. Thus, activation of p38 SAPK is critical to elicit the early gene expression program required for cell adaptation to stress.
Resumo:
All ontogenetic stages of a life cycle are exposed to environmental conditions so that population persistence depends on the performance of both adults and offspring. Most studies analysing the influence of abiotic conditions on species performance have focussed on adults, while studies covering early life-history stages remain rare. We investigated the responses of early stages of two widely introduced ascidians, Styela plicata and Microcosmus squamiger, to different abiotic conditions. Stressors mimicked conditions in the habitats where both species can be found in their distributional ranges and responses were related to the selection potential of their populations by analysing their genetic diversity. Four developmental stages (egg fertilisation, larval development, settlement, metamorphosis) were studied after exposure to high temperature (30°C), low salinities (26 and 22 ) and high copper concentrations (25, 50 and 100 µg/L). Although most stressors effectively led to failure of complete development (fertilisation through metamorphosis), fertilisation and larval development were the most sensitive stages. All the studied stressors affected the development of both species, though responses differed with stage and stressor. S. plicata was overall more resistant to copper, and some stages of M. squamiger to low salinities. No relationship was found between parental genetic composition and responses to stressors. We conclude that successful development can be prevented at several life-history stages, and therefore, it is essential to consider multiple stages when assessing species' abilities to tolerate stress. Moreover, we found that early development of these species cannot be completed under conditions prevailing where adults live. These populations must therefore recruit from elsewhere or reproduce during temporal windows of more benign conditions. Alternatively, novel strategies or behaviours that increase overall reproductive success might be responsible for ensuring population survival.
Resumo:
Cells are subjected to dramatic changes of gene expression upon environmental changes. Stresscauses a general down-regulation of gene expression together with the induction of a set of stress-responsivegenes. The p38-related stress-activated protein kinase Hog1 is an important regulator of transcription uponosmostress in yeast. Genome-wide localization studies of RNA polymerase II (RNA Pol II) and Hog1 showed that stress induced major changes in RNA Pol II localization, with a shift toward stress-responsive genes relative to housekeeping genes. RNA Pol II relocalization required Hog1, which was also localized to stress-responsive loci. In addition to RNA Pol II-bound genes, Hog1 also localized to RNA polymerase III-bound genes, pointing to a wider role for Hog1 in transcriptional control than initially expected. Interestingly, an increasing association of Hog1 with stressresponsive genes was strongly correlated with chromatin remodeling and increased gene expression. Remarkably, MNase-Seq analysis showed that although chromatin structure was not significantly altered at a genome-wide level in response to stress, there was pronounced chromatin remodeling for those genes that displayed Hog1 association. Hog1 serves to bypass the general down-regulation of gene expression that occurs in response to osmostress, and does so both by targeting RNA Pol II machinery and by inducing chromatin remodeling at stressresponsive loci.