Deleterious gene interactions due to accumulation of individual genetic variations between different lineages are a cause of population diversification by creating reproductive barriers that ultimately lead to differentiation of species. One type of deleterious interactions is called “hybrid necrosis”, in which epistatic interactions between some plant immunity genes (usually very variable) cause autoimmunities that produce a necrotic and dwarf phenotype. Hybrid necrosis has been widely studied in several plant species, such as Arabidopsis thaliana and many gene interactions were found for that plant. This study tests the applicability of these results on a close relative, A. lyrata, by crossing individuals from different populations and genotyping F2 progeny with polymorphic markers close to homologous sequences to those involved in hybrid necrosis in A. thaliana. Results suggest the possibility of a homologous gene to DM8 or DM9 in chromosome 7 to be involved in formation of hybrid necrosis.

No description available.

Temperate tree species exhibit seasonal growth cycling, and the timing of such transition varies with local climate. Under anthropogenic climate change, the local pattern of growth and dormancy in tree populations is expected to become uncoupled with shifting seasonal environmental signals, particularly temperature. Thus, an understanding of the genetic underpinnings of local adaptation is key to predicting the fate of tree populations in the future. In this thesis, we coupled sampling of range-wide natural accessions of P. trichocarpa with adaptive trait phenotyping and genome-wide genotyping to uncover relationships between genotype, phenotype, and environment. We detected strong correlations between adaptive phenotypes, climate, and geography, which suggested climatic selection driving adaptation of these populations to local environments. We subsequently combined genotype-phenotype association tests with sliding window analysis and identified regions strongly associated with these adaptive traits. We also compared adaptive markers identified in two independent GWAS on samples across latitude and altitude transects and found a set of associated variants shared across both transects. We further scanned the genome with three selection tests to identify regions showing evidence of recent positive and divergent selection. By comparing candidate selection regions across altitude and latitude, we detected a set of overlapping regions showing differentiation across gradients of the same climate variables. We validated the functional imortance of these selection regions by combining GWAS and showed that selection regions contain a strong signature of phenotypic associations. We also studied the distribution of deleterious allels across genome and natural populations, and found that deleterious alleles preferentially accumulate in regions of low recombination and hithihking regions. Finally, marginal populations contained more deleterious alleles compared with central populations, which is likely due to ineffective selection in small populations and recent bottlenecks associated with postglacial recolonization. These findings provide new insights into the genomic architecture underlying climatic adaptation and how selection drives adaptive evolution of tree species. / Ph. D.

[EN] Our understanding of the biological mechanisms for most common human diseases is far from complete. Even with well established genetic landscapes, our capacity to make accurate phenotypical predictions or determine personalised disease risk using genetics alone is not possible for most diseases due to our lack of understanding of the mechanisms by which genetic alterations cause disease. Several suggestions have been proposed to explain this manifested lack of direct relation between genotype and phenotype, including interactions with other molecules, pleiotropy and environmental perturbations. Due to their essential role in carrying cellular functions, proteins and its interactions seem crucial to translate genomic data to phenotypic states. In this thesis I present three different and independent approaches to integrate human genomic data with prior knowledge in terms of protein-protein interactions (PPIs). The overall objective is, by making use of the interactome structure, to propose functional hypotheses that help to interpret the genetic variability observed in different human phenotypes. First I developed a methodology to extract the network component associated to any gene list ranked by any experimental parameter, as the one coming from case-control genome-wide associations studies. Second I performed a systematic analysis of human variants in the context of the protein interactome. There I study how the interactome structure can help us to explain the amount of apparently deleterious variation observed in actual populations and, therefore, give insight in its role in shaping the patterns of variability. Results are compared against somatic mutation found in Leukemia patients. Finally, I structurally resolved the protein interactome and used it to study how somatic mutations found in primary tumours distribute across the interacting interfaces and identify those with a potential role in driving oncogenesis. Although each chapter covers a different question, all of them demonstrate the potential of the interactome in helping to interpret genomic variation observed under diverse research scenarios. / [ES] Nuestro conocimiento acerca de los mecanismos biológicos causantes de la mayoría de enfermedades humanas comunes es aun pobre. Incluso con mapas genéticos de alta resolución, nuestra capacidad para hacer predicciones fenotípicas certeras o determinar el riesgo de una persona a padecer una enfermedad utilizando solamente marcadores genéticos es muy baja. Entre las principales causas de esta aparente falta de relación directa entre genotipo y fenotipo están las interacciones moleculares, los fenómenos de pleiotropía y la influencia de los factores externos. Debido al papel esencial que ejercen en llevar a cabo las funciones celulares, las proteínas y sus interacciones han adquirido una atención especial en la traducción de los datos genotípicos a estados fenotípicos. En esta tesis se presentan tres estrategias diferentes para la integración de datos genómicos humanos con la red de interacciones proteicas (interactoma). El objetivo común de todas ellas es, haciendo uso de la estructura del interactoma, proponer hipótesis funcionales que ayuden a interpretar los patrones de variabilidad observados en diferentes estados fenotípicos humanos. Primero, se propone una metodología para extraer el componente del interactoma asociado a los genes relevantes en una lista ranqueada por cualquier parámetro experimental, como el estadístico derivado de los estudios de asociación genómicos. Es segundo lugar se describe un análisis sistemático de las variantes genéticas observadas en humanos sanos en el contexto del interactoma. En él se estudia cómo la estructura del interactoma puede ayudar en explicar la aparentemente elevada cantidad de variantes deletéreas observadas en los últimos estudios poblacionales de secuenciación de genomas. Los resultados son comparados con las mutaciones somáticas observadas en pacientes de Leucemia. Finalmente, se presenta un estudio de las mutaciones somáticas observadas en tumores primarios utilizando una versión del interactoma que incluye la estructura tridimensional de las proteínas. Aunque cada estudio presentado en la tesis pretende resolver preguntas diferentes, todos ellos demuestran el potencial del interactoma de proteínas en ayudar a interpretar la variación genómica humana observada en un contexto tanto evolutivo como de enfermedad. / [CA] El nostre coneixement sobre els mecanismes biològics causants de la majoria de malalties humanes comuns es encara pobre. Tot i que en l'actualitat tenim mapes genètics d'alta resolució, la nostra capacitat per a fer prediccions fenotípiques certeres utilitzant únicament marcadors genètics es encara molt baixa degut a que no entenem les bases moleculars a traves de les quals les alteracions genètiques condicionen un fenotip de malaltia. Entre les principals causes d'aquesta aparent falta de relació directa entre genotip i fenotip estan la complexitat introduïda per les interacciones moleculars, els fenòmens de peleiotropia i la influencia dels factors externs. Degut al paper clau en dur a terme la majoria de funcions cel·lulars, les proteïnes i les seues interaccions han adquirit una especial atenció en la traducció de les dades genotípiques en estats fenotípics. Aquesta tesi presenta tres estartègies diferents per a la integració de dades genòmiques humanes amb la xarxa d'interaccions proteiques (interactoma). L'objectiu comú es, fent ús de l'estructura del interactoma, proposar hipòtesis funcionals que ajuden a interpretar els patrons de variabilitat genètica observats en diferents estats fenotípics. En primer lloc, es proposa una metodologia per a extraure el component de l'interactoma associat als gens rellevants en una llista ranquejada per qualsevol paràmetre experimental, com l'estadístic derivat d'estudis d'assocaició de genoma. En segon lloc, es descriu un anàlisi sistemàtic de les variants genètiques observades en humans sans en el context del interactoma. Ací s'analitza com l'estructura del interactoma pot ajudar a explicar l'aparent elevada quantitat de variants deletèries observades en els últims estudis poblacionals de sequenciació de genomes. Els resultats son comparats amb les mutacions somàtiques observades en pacients de Leucèmia. Finalment, es presenta un estudi de les mutacions somàtiques observades en tumors primaris de més de 20 tipus utilitzant una versió del interactoma més resolutiva, que inclou l'estructura tridimensional de les proteïnes. Encara que cada estudi presentat en la tesi planteja resoldre qüestions diferents, tots ells demostren el potencial del interactoma de proteïnes en ajudar a interpretar la variació genòmica humana observada en un context tant poblacional com de malaltia. / García Alonso, LM. (2015). Functional profiling of human genomic data using the protein interactome [Tesis doctoral]. Universitat Politècnica de València. https://doi.org/10.4995/Thesis/10251/55848

É o processo de mutação que, em última instância, introduz diversidade nas populações. Quando a mutação é pontual e segrega na população, recebe o nome de polimorfismo de nucleotídeo único (ou SNP, de Single Nucleotide Polymorphism). Caso esse SNP seja vantajoso, ele aumenta de frequência na população e estabelece um forte desequilíbrio de ligação com seus SNPs vizinhos, consequência do processo chamado de efeito de carona genética. Esse efeito pode ter duas consequências na proximidade dos sítios selecionados: (1) pode levar ao aumento de frequência de mutações neutras ligadas a mutação vantajosa ou (2) pode reduzir o tamanho efetivo da população Ne nessas regiões, e, consequentemente aumentar a importância da deriva genética na variação genética dessas regiões. Como consequência, é comum que a região próxima a sítios vantajosos apresente acúmulo de mutações neutras com frequências acima do esperado sob neutralidade. No entanto, a maior parte de novas mutações são deletérias e seria esperado que fossem removidas da população por seleção purificadora. Entretanto, como os padrões de variabilidade observados no genoma resultam de processos seletivos atuando em conjunto com a deriva genética, não é incomum SNPs fracamente deletérios atingirem frequências elevadas nos diferentes contextos de história demográfica e seletiva das populações. O acúmulo desses SNPs fracamente deletérios no genoma reduz progressivamente a aptidão média da população, o que representa um aumento de sua carga genética. Neste estudo investigamos se na vizinhança de sítios vantajosos selecionados há um acúmulo de SNPs deletérios, contribuindo para a carga genética da população. Para responder essa questão, dividimos nosso estudo em três passos. Primeiro, desenvolvemos uma nova metodologia para estimar a diferença na carga genética entre região vizinha a sítios selecionados e o resto do genoma. Nossa metodologia é mais robusta do que a tradicionalmente utilizada pois garante que a região influenciada pela seleção natural e o controle apresentem o mesmo número de SNPs, e possibilita controlar para variáveis confundidoras, como a frequência dos polimorfismos, permitindo explorar regiões alvo com diferentes características e reduzir resultados espúrios. Em seguida, utilizamos nossa metodologia para testar se a carga genética na região vizinha a sítios sob seleção positiva é maior do que no restante do genoma. Identificamos um acúmulo de SNPs deletérios em europeus e leste asiáticos para amostras do projeto 1000 genomas.Mostramos também que as mesmas regiões exploradas em populações sob efeito de seleção positiva não apresentaram carga genética aumentada em populações nas quais essas regiões não experimentaram seleção positiva. Por último, utilizamos essa mesma metodologia para avaliar a carga genética em genes sob seleção balanceadora, os genes clássicos do HLA de classe I. Esses genes compõe uma das famílias gênicas mais estudadas em humanos e para os quais existem evidências indicando os sítios específicos que estão sob seleção balanceadora. Nosso teste mostrou que as regiões vizinhas aos sítios sob seleção balanceadora dentro dos genes do HLA apresentam acúmulo de SNPs deletérios para pelo menos dois agrupamentos populacionais. Assim, com os três passos aqui descritos, conseguimos apontar o aumento da carga genética em regiões próximas a sítios sob dois regimes de seleção distintos, utilizando uma metodologia capaz de considerar características específicas das regiões estudadas / It is the mutation process that ultimately introduces diversity into populations. When a mutation is punctual and segregates in the population, it is called a single nucleotide polymorphism (SNP). If this mutation is advantageous, it increases in frequency in the population and creates strong linkage disequilibrium with its neighboring loci, as a consequence of the hitchhiking effect. This effect can have two consequences in the vicinity of the selected sites: (1) it can increase the frequency of neutral mutations linked to this advantageous mutation or (2) can reduce the effective population size Ne in the region around the selected site, and consequently increase the importance of genetic drift in the genetic variation of these regions. As a consequence, it is common that the region around sites under advantageous selection to accumulate more neutral mutations at high frequencies than expected under neutrality. However, most new mutation are deleterious and it is expected that these mutation will be removed from the population by purifying selection. However, since the patterns of variability observed in the genome result from selective processes interacting with genetic drift, it is common for weakly deleterious SNPs to reach high frequencies in different population demographic histories. The accumulation of these weakly deleterious SNPs in the genome progressively reduces the population\'s fitness, increasing their genetic load. In this study we investigated whether in the neighborhood of selected sites there is an accumulation of deleterious SNPs due to hitchhiking, contributing to the genetic load of the population. To answer this question, we divided our study into three steps. First, we developed a new methodology to estimate the genetic load difference between the region around selected sites and the rest of the genome. Our methodology is more robust than those traditionally used one because it ensures that both the region influenced by natural selection and control have the same number of SNPs, reducing the probability of spurious results, and is flexible to different genome peculiarities, making it possible to explore target regions with different characteristics. We then used our methodology to test whether genetic load in the region around sites under positive selection is greater than in the rest of the genome. We found consistent evidence of an accumulation of deleterious SNPs in European and East Asian continental groups. We also showed that these same region do not present the same deleterious SNP accumulation in populations in which these region did not experience positive selection. Finally, we used this same methodology to evaluate the genetic load in genes under the balancing selection, the classic HLA class I genes. These genes are one of the most studied in humans and there is evidence that indicates the specific sites within these genes that are under balancing selection. We found that the regions around these sites under balancing selection within the HLA genes had deleterious SNPs accumulating for at least two continental groups. Thus, with the three steps described here, we were able to point out the increase of genetic load in regions around selected sites for two distinct selective regimes using a methodology that takes into account specific characteristics of the studied regions

<p><i>Paenibacillus polymyxa</i> belongs to the group of plant growth promoting rhizobacteria (PGPR). Activities associated with <i>P. polymyxa</i>-treatment of plants in earlier experiments include, e.g., nitrogen fixation, soil phosphorus solubilization, production of antibiotics, auxin, chitinase, and hydrolytic enzymes, as well as promotion of increased soil porosity. My thesis work showed that, in stationary phase, <i>P. polymyxa</i> released the plant hormone cytokinin isopentenyladenine, in concentrations of about 1.5 nM.</p><p>In a gnotobiotic system with <i>Arabidopsis thaliana</i> as a model plant, it was shown that <i>P. polymyxa</i>-inoculation protects plants; challenge by either the pathogen <i>Erwinia carotovora</i> (biotic stress) or induction of drought (abiotic stress) showed that pre-inoculated plants were significantly more resistant than control plants. By RNA-differential display on RNA from <i>P. polymyxa</i>-treated or control plants, changes in gene expression were tested. One mRNA, encoding ERD15 (drought stress-responsive gene) showed a strong inoculation-dependent increase in abundance. In addition, several biotic stress-related genes were also activated by <i>P. polymyxa</i>. </p><p>Antagonism towards the fungal pathogens <i>Phytophthora palmivora</i> and <i>Pythium aphanidermatum</i> was studied. <i>P. polymyxa</i> counteracted the colonization of zoospores of both oomycetes on <i>A. thaliana</i> roots, and survival rates of plants treated with <i>P. polymyxa</i> were much higher when challenged by <i>P. aphanidermatum</i>. </p><p>Using a green fluorescent protein-tagged isolate of <i>P. polymyxa</i>, colonization of <i>A. thaliana</i> roots was investigated. Two main conclusions can be drawn. Firstly, the bacterium enters the root tissue (but not leaves) and is abundantly present in intercellular spaces. Secondly, the root becomes severely damaged, indicating that – under some conditions – <i>P. polymyxa</i> is a "deleterious bacterium", and in others it promotes growth. Based on work presented in my thesis, I argue that a balance between the activities of a PGPR, the genetic background and physiological state of a plant, and the environmental conditions employed in test systems, ultimately determines the resulting effect. </p>

Paenibacillus polymyxa belongs to the group of plant growth promoting rhizobacteria (PGPR). Activities associated with P. polymyxa-treatment of plants in earlier experiments include, e.g., nitrogen fixation, soil phosphorus solubilization, production of antibiotics, auxin, chitinase, and hydrolytic enzymes, as well as promotion of increased soil porosity. My thesis work showed that, in stationary phase, P. polymyxa released the plant hormone cytokinin isopentenyladenine, in concentrations of about 1.5 nM. In a gnotobiotic system with Arabidopsis thaliana as a model plant, it was shown that P. polymyxa-inoculation protects plants; challenge by either the pathogen Erwinia carotovora (biotic stress) or induction of drought (abiotic stress) showed that pre-inoculated plants were significantly more resistant than control plants. By RNA-differential display on RNA from P. polymyxa-treated or control plants, changes in gene expression were tested. One mRNA, encoding ERD15 (drought stress-responsive gene) showed a strong inoculation-dependent increase in abundance. In addition, several biotic stress-related genes were also activated by P. polymyxa. Antagonism towards the fungal pathogens Phytophthora palmivora and Pythium aphanidermatum was studied. P. polymyxa counteracted the colonization of zoospores of both oomycetes on A. thaliana roots, and survival rates of plants treated with P. polymyxa were much higher when challenged by P. aphanidermatum. Using a green fluorescent protein-tagged isolate of P. polymyxa, colonization of A. thaliana roots was investigated. Two main conclusions can be drawn. Firstly, the bacterium enters the root tissue (but not leaves) and is abundantly present in intercellular spaces. Secondly, the root becomes severely damaged, indicating that – under some conditions – P. polymyxa is a "deleterious bacterium", and in others it promotes growth. Based on work presented in my thesis, I argue that a balance between the activities of a PGPR, the genetic background and physiological state of a plant, and the environmental conditions employed in test systems, ultimately determines the resulting effect.

Most clonal plants exhibit a modular structure at multiple levels. At the level of the organs, they are characterized by functional modules, such as, internodes, leaves, branches. At the level of the genetic individual (clone or genet), they possess independent evolutionary and physiological units (ramets). These evolutionary units arise through the widespread phenomenon of clonal reproduction, achieved in a variety of ways including rhizomes, stolons, bulbils, or lateral roots. The focus of this study was Populus tremuloides, trembling aspen, a dioecious tree that reproduces sexually by seed and asexually through lateral roots. Local forest patches in western populations of Populus tremuloides consisted largely of multiple genotypes. Multi-clonal patches were dominated by a single genotype, and in one population (Riske Creek) we found several patches (five out of 17) consisting of a single genotype. A second consequence of modularity is that during the repeated cycle of ramet birth, development and death, somatic mutations have the opportunity to occur. Eventually, the clone becomes a mosaic of mutant and non-mutant cell lineages. We found that neutral somatic mutations accumulated across 14 microsatellite loci at a rate of between 10^-6 and 10^-5 per locus per year. We suggest that neutral genetic divergence, under a star phylogeny model of clonal growth, is an alternative way to estimate clone age. Previous estimates of clone age couple the mean growth rate per year of shoots with the area covered by the clone. This assumes a positive linear relationship between clone age and clone size. We found, however, no repeatable pattern across our populations in terms of the relationship of either shape or size to the number of somatic changes. A final consequence of modularity is that during clonal growth, natural selection is relaxed for traits involving sexual function. This means that mutations deleterious to sexual function can accumulate, reducing the overall sexual fitness of a clone. We coupled neutral genetic divergence within clones with pollen fitness data to infer the rate and effect of mildly deleterious mutations. Mutations reduced relative sexual fitness in clonal aspen populations by about 0.12x10^-3 to 1.01x10^-3 per year. Furthermore, the decline in sexual function with clone age is evidence that clonal organisms are vulnerable to the effects of senescence.

Most clonal plants exhibit a modular structure at multiple levels. At the level of the organs, they are characterized by functional modules, such as, internodes, leaves, branches. At the level of the genetic individual (clone or genet), they possess independent evolutionary and physiological units (ramets). These evolutionary units arise through the widespread phenomenon of clonal reproduction, achieved in a variety of ways including rhizomes, stolons, bulbils, or lateral roots. The focus of this study was Populus tremuloides, trembling aspen, a dioecious tree that reproduces sexually by seed and asexually through lateral roots. Local forest patches in western populations of Populus tremuloides consisted largely of multiple genotypes. Multi-clonal patches were dominated by a single genotype, and in one population (Riske Creek) we found several patches (five out of 17) consisting of a single genotype. A second consequence of modularity is that during the repeated cycle of ramet birth, development and death, somatic mutations have the opportunity to occur. Eventually, the clone becomes a mosaic of mutant and non-mutant cell lineages. We found that neutral somatic mutations accumulated across 14 microsatellite loci at a rate of between 10^-6 and 10^-5 per locus per year. We suggest that neutral genetic divergence, under a star phylogeny model of clonal growth, is an alternative way to estimate clone age. Previous estimates of clone age couple the mean growth rate per year of shoots with the area covered by the clone. This assumes a positive linear relationship between clone age and clone size. We found, however, no repeatable pattern across our populations in terms of the relationship of either shape or size to the number of somatic changes. A final consequence of modularity is that during clonal growth, natural selection is relaxed for traits involving sexual function. This means that mutations deleterious to sexual function can accumulate, reducing the overall sexual fitness of a clone. We coupled neutral genetic divergence within clones with pollen fitness data to infer the rate and effect of mildly deleterious mutations. Mutations reduced relative sexual fitness in clonal aspen populations by about 0.12x10^-3 to 1.01x10^-3 per year. Furthermore, the decline in sexual function with clone age is evidence that clonal organisms are vulnerable to the effects of senescence.

CoordenaÃÃo de AperfeÃoamento de Pessoal de NÃvel Superior / The great demand for techniques that can detect and determine the degree of susceptibility to corrosion motivated thedevelopment of a research project that resulted in the construction of a portable electrochemical cell that has been validated according to ASTM A262. The success of this technique for nondestructive evaluation has motivated the expansion of this technique to other materials and phenomena of precipitation. In this work it was evaluated the use of this EPR-DL portable cell used applied for assessing the susceptibility to corrosion in super duplex stainless steels UNSS32750 and UNSS32760.Those materials were heat treated at 475ÂC and 850ÂC at different time of creating different patterns precipitation of deleterious phases to be detected by the cell. The solutions used were: 2M H2SO4 +0.01 M KSCN +0.5 M NaCl (solution 1 ) and 2M H2SO4 +0.01 M KSCN +1.0 M NaCl (solution 2) and the speedsscanswerestudied: 1.67 mV / s , 3.0 mV / s and 6.0 mV / s. To prove the presence of deleterious phases precipitation and associate them with the electrochemical behavior presentedby the electrochemical cell, the sampleshad theirmicrostructuresanalyzedby optical microscopy (OM), scanning electron microscopy (SEM), and energy dispersive of X-ray spectroscopy (EDS). Also the consumption of ferrite magnetic phase was assessed with ferrite scope and performed Vickers hardness tests to analyze the increasing in hardness due to precipitation of deleterious phases. It was observed by OM, SEM / EDS, ferrite scope, EPR- DL and Vickers hardness, that as much longer the heat treatment the amount of deleterious phasesprecipitated was increased. The results demonstrated that the solution 2 was the most effective in detecting susceptibility to corrosion, being capable to detect the depletion of chromium even in conditions of low precipitation and obtaining greater values of Ir/Ia as the scanning speed was reduced to the same condition of heat treatment. All these analyzes has confirmed that the EPR- DL portable cell was able to detect the depletionof chromium caused by the presence of deleterious phases, and reflecting the degree of susceptibility to corrosion of SDSS which were studied / A grande demanda por tÃcnicas que consigam detectar e determinar o grau de susceptibilidade à corrosÃo motivou o desenvolvimento de um projeto que resultou na construÃÃo de uma cÃlula portÃtil para a determinaÃÃo do fenÃmeno da sensitizaÃÃo em aÃos inoxidÃveis austenÃticos, a qual foi validada seguindo a norma ASTM A262. O sucesso desta tÃcnica nÃo destrutiva em campo tem motivado a expansÃo dessa tÃcnica de anÃlise para outros materiais e fenÃmenos de precipitaÃÃo. O presente trabalho apresenta a avaliaÃÃo dessa cÃlula portÃtil utilizada em ensaios de EPRâDL para avaliaÃÃo de susceptibilidade a corrosÃo nos AISD UNS S32750 e UNS S32760. Estes materiais foram tratados termicamente a 475ÂC e a 850ÂCem diferentes tempos, criando diferentes padrÃes de precipitaÃÃes de fases deletÃrias para serem detectados pela cÃlula. As soluÃÃes utilizadas foram: 2M de H2SO4+0,01M de KSCN+0,5 M de NaCl (soluÃÃo 1) e 2M de H2SO4+0,01M de KSCN+1,0 M de NaCl (soluÃÃo2) e as velocidades de varreduras estudadas foram de 1,67mV/s, 3,0mV/s e 6,0mV/s. Para comprovar a presenÃa da precipitaÃÃo de fases deletÃrias e associÃ-las ao comportamento eletroquÃmico apresentado pela cÃlula, as amostras tiveram suas microestruturas analisadas por microscopia Ãtica (MO), microscopia eletrÃnica de varredura (MEV),e ensaios com energia dispersiva de raios-X (EDS).TambÃm foram avaliados o consumo da fase ferrita por analise magnÃtica com ferritoscÃpio e realizados ensaios de dureza Vickers para analisar o aumento da dureza devido a precipitaÃÃo das fases deletÃrias. Foi observado por MO, MEV/ EDS, ferritoscÃpio, EPR-DL e por dureza Vickers que quando maior o tempo de tratamento tÃrmico maior foi a quantidade de fases deletÃrias precipitadas. Quanto maior foi o nÃvel de precipitaÃÃo, maiores foram os valores de Ir/Ia e maiores valores de dureza foram obtidos. Os resultados mostraram que a soluÃÃo 2 foi a mais eficaz na detecÃÃo da susceptibilidade a corrosÃo, conseguindo detectar o empobrecimento de cromo mesmo em condiÃÃes de baixa precipitaÃÃo, e obtendo maior valores de Ir/Ia conforme a velocidade de varredura era diminuÃda para uma mesma condiÃÃo de tratamento. Todas essas anÃlises comprovaram que a cÃlula portÃtil de EPR- DL foi capaz de detectar o empobrecimento de cromo ocasionado pela presenÃa das fases deletÃrias, e refletindo o grau de susceptibilidade a corrosÃo dos AISD estudados.