Academic literature on the topic 'Mutagenesis'

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Journal articles on the topic "Mutagenesis"

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Gupta, Neha, Megha Malu, and Aparajita Beera. "Mutagenesis." International Journal of Oral Care & Research 5, no. 3 (2017): 252–56. http://dx.doi.org/10.5005/jp-journals-10051-0109.

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Natarajan, A. T. "Mutagenesis." Cytogenetic and Genome Research 81, no. 2 (1998): 159–64. http://dx.doi.org/10.1159/000015017.

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Symonds, Neville. "Anticipatory mutagenesis?" Nature 337, no. 6203 (January 1989): 119–20. http://dx.doi.org/10.1038/337119a0.

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Novak, Kris. "Meningococcal mutagenesis." Nature Biotechnology 18, no. 11 (November 2000): 1129. http://dx.doi.org/10.1038/81060.

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Weitzman, Jonathan. "Minos mutagenesis." Genome Biology 1 (2000): spotlight—20001128–01. http://dx.doi.org/10.1186/gb-spotlight-20001128-01.

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Weitzman, Jonathan B. "Mouse mutagenesis." Genome Biology 3 (2002): spotlight—20020226–01. http://dx.doi.org/10.1186/gb-spotlight-20020226-01.

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Murli, Sumati, and Graham C. Walker. "SOS mutagenesis." Current Opinion in Genetics & Development 3, no. 5 (October 1993): 719–25. http://dx.doi.org/10.1016/s0959-437x(05)80089-9.

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Vainio, Harri. "Environmental mutagenesis." Molecular Medicine Today 2, no. 9 (September 1996): 370–71. http://dx.doi.org/10.1016/s1357-4310(96)80010-4.

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Antalis, T. "Serpin mutagenesis." Methods 32, no. 2 (February 2004): 130–40. http://dx.doi.org/10.1016/s1046-2023(03)00204-4.

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Fawcett, H. H. "Environmental mutagenesis." Journal of Hazardous Materials 10, no. 1 (February 1985): 152. http://dx.doi.org/10.1016/0304-3894(85)80013-3.

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Dissertations / Theses on the topic "Mutagenesis"

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Martin, Stephen Lewis. "Novel methods for mutagenesis." Thesis, University of Oxford, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.302789.

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Ennis, Don Gregory. "Genetics of SOS mutagenesis." Diss., The University of Arizona, 1988. http://hdl.handle.net/10150/184602.

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Previous genetic evidence suggested that RecA was required in SOS mutagenesis for its regulatory role and perhaps some other nonregulatory role (Mount, 1977; Blanco et al., 1982). I undertook a genetic study which confirmed the above studies and provided further evidence that RecA protein appeared to have a dual "role in mutagenesis; first, the cleavage of LexA repressor for the derepression of specific SOS genes and second, one or more additional role(s). For these studies a new phage mutagenesis assay was developed which allows rapid scoring of SOS mutagenesis in a large number of host mutants. I next conducted a genetic analysis to determine if the newly defined RecA mutagenesis function was separable by mutation from the numerous other phenotypes which are known to be influenced by RecA protein. From the study of recA mutants it appears that the RecA mutagenesis function(s) is genetically separable from the following RecA phenotypes: LexA cleavage, lambda cI repressor cleavage, UV resistance and homologous recombination. In addition, I discovered that the LexA cleavage function and lambda cI cleavage function is also separable. I also studied in some detail the novel genetic properties that I uncovered for recA432 mutant strains. recA432 was defined as a mutagenesis defective allele (Kato and Shinoura, 1977). LexA cleavage in recA432 cells was more easily induced that in recA⁺ cells, causing lethal filamentation of these mutant cells even at very low UV doses. I concluded that the basis for the Mut⁻ phenotype was this strain's propensity to lethally filament, which complicated the detection of mutant cells. In another set of experiments, I examined the regulatory requirements for SOS mutagenesis and Weigle phage-reactivation; I wanted to determine which SOS operons must be derepressed for this process. lexA(Ind⁻) mutant cells are defective in mutagenesis because they cannot derepress specific SOS genes required in this process. I found that the selective derepression of umuDC was sufficient to restore mutagenesis to these lexA(Ind⁻) mutants; however, derepression of umuDC and recA was required for phage reactivation.
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Porto, Marília de Paula [UNESP]. "Ação moduladora do citral e eugenol em eventos genéticos em magrófagos murinos in vitro." Universidade Estadual Paulista (UNESP), 2012. http://hdl.handle.net/11449/92460.

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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
Devido a propriedades terapêuticas, várias plantas e seus constituintes químicos vêm sendo muitas vezes utilizados como o primeiro recurso para o tratamento de diversas doenças. Nesse contexto, compostos isolados de plantas têm sido alvos de inúmeros estudos que avaliam, além da atividade, seus possíveis mecanismos de ação. Dentre os compostos com potencial quimioprotetor, o citral e o eugenol merecem atenção devido suas estruturas químicas de monoterpeno e de composto fenólico, respectivamente, e por seus potenciais anti-inflamatório, antiparasitário e antioxidante. Considerando que mutação no DNA pode ser a primeira etapa de várias doenças, e que lesões induzidas nessa molécula podem ser prevenidas ou moduladas por compostos naturais, este estudo objetivou avaliar, pelo teste do cometa, o potencial genotóxico do citral (25, 50 e 100 Tg/mL) e do eugenol (0,31, 0,62, 1,24 e 2,48 Tg/mL), após diferentes tempos de tratamento (6, 10, 24 e 30 h) e, também, seus possíveis efeitos moduladores sobre danos induzidos no DNA pela doxorrubicina (DOX), em diferentes protocolos de tratamento (pré, pós e simultaneamente à DOX) e momentos de análise (12, 24 e 36 h), em macrófagos peritoneais de camundongos. Além disso, foi avaliado o potencial toxicogenômico do citral e do eugenol por meio da modulação da expressão dos genes NF-kB1, COX-2 e TNF-α (relacionados a processos inflamatórios) em macrófagos ativados ou não por lipopolissacarideo de bactéria (LPS). Os resultados mostraram que ambos os compostos apresentaram potencial genotóxico. No caso do citral, a genotoxicidade foi observada para as duas maiores concentrações, mas apenas no tempo de 6h; para o eugenol, o aumento de danos no DNA foi detectado para todas as concentrações, em pelo menos um momento de análise. Com relação ao potencial...
Because of the therapeutic properties, several plants and their chemical constituents have been used for treatment of various diseases. Therefore, isolated compounds from plants have been targets of numerous studies that evaluate their activity and mechanisms of action. Among compounds with chemopreventive potential, citral and eugenol have gain attention because of their chemical structures, monoterpene and phenol,respectively, and for their anti-inflammatory, antioxidant and antiparasitic potentials. Since DNA mutation is the first step for some diseases, and since the lesions induced in this molecule can be prevented or modulated by natural compounds, aim of the present study was first to evaluate the genotoxic potential of citral (25, 50 and 100 Tg/mL) and eugenol (0.31, 0.62, 1.24 and 2.48 Tg/mL) at different times after exposure (6, 10, 24 and 30 h), and then, their ability to modulate DNA damage induced by doxorubicin (DOX) at different treatment protocols (pre, post and simultaneous with DOX) and times (12, 24 and 36 h) in mice peritoneal macrophages. In addition, the toxicogenomic potential of citral and eugenol by modulating the expression of NF-KB1, COX-2 and TNF-α (related to inflammatory processes) genes in macrophages activated or not by bacterial lipopolysaccharide (LPS) was also investigated. The results showed that both compounds have genotoxic potential. In the case of citral, genotoxicity was observed for the two major concentrations, but only 6h after the exposure. For eugenol, increased DNA damage was detected for all concentrations, in at least one moment of analysis. Related to the antigenotoxicity, both citral and eugenol presented protective effects at different concentrations and treatment protocols, and the more effective activities were detected at simultaneous and pre-treatment... (Complete abstract click electronic access below)
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Porto, Marília de Paula. "Ação moduladora do citral e eugenol em eventos genéticos em magrófagos murinos in vitro /." Botucatu : [s.n.], 2012. http://hdl.handle.net/11449/92460.

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Orientador: Daisy Maria Fávero Salvadori
Coorientador: Glenda Nicioli da Silva
Banca: Luís Fernando Barbisan
Banca: Denise Crispim Tavares
Resumo: Devido a propriedades terapêuticas, várias plantas e seus constituintes químicos vêm sendo muitas vezes utilizados como o primeiro recurso para o tratamento de diversas doenças. Nesse contexto, compostos isolados de plantas têm sido alvos de inúmeros estudos que avaliam, além da atividade, seus possíveis mecanismos de ação. Dentre os compostos com potencial quimioprotetor, o citral e o eugenol merecem atenção devido suas estruturas químicas de monoterpeno e de composto fenólico, respectivamente, e por seus potenciais anti-inflamatório, antiparasitário e antioxidante. Considerando que mutação no DNA pode ser a primeira etapa de várias doenças, e que lesões induzidas nessa molécula podem ser prevenidas ou moduladas por compostos naturais, este estudo objetivou avaliar, pelo teste do cometa, o potencial genotóxico do citral (25, 50 e 100 Tg/mL) e do eugenol (0,31, 0,62, 1,24 e 2,48 Tg/mL), após diferentes tempos de tratamento (6, 10, 24 e 30 h) e, também, seus possíveis efeitos moduladores sobre danos induzidos no DNA pela doxorrubicina (DOX), em diferentes protocolos de tratamento (pré, pós e simultaneamente à DOX) e momentos de análise (12, 24 e 36 h), em macrófagos peritoneais de camundongos. Além disso, foi avaliado o potencial toxicogenômico do citral e do eugenol por meio da modulação da expressão dos genes NF-kB1, COX-2 e TNF-α (relacionados a processos inflamatórios) em macrófagos ativados ou não por lipopolissacarideo de bactéria (LPS). Os resultados mostraram que ambos os compostos apresentaram potencial genotóxico. No caso do citral, a genotoxicidade foi observada para as duas maiores concentrações, mas apenas no tempo de 6h; para o eugenol, o aumento de danos no DNA foi detectado para todas as concentrações, em pelo menos um momento de análise. Com relação ao potencial... (Resumo completo, clicar acesso eletrônico abaixo)
Abstract: Because of the therapeutic properties, several plants and their chemical constituents have been used for treatment of various diseases. Therefore, isolated compounds from plants have been targets of numerous studies that evaluate their activity and mechanisms of action. Among compounds with chemopreventive potential, citral and eugenol have gain attention because of their chemical structures, monoterpene and phenol,respectively, and for their anti-inflammatory, antioxidant and antiparasitic potentials. Since DNA mutation is the first step for some diseases, and since the lesions induced in this molecule can be prevented or modulated by natural compounds, aim of the present study was first to evaluate the genotoxic potential of citral (25, 50 and 100 Tg/mL) and eugenol (0.31, 0.62, 1.24 and 2.48 Tg/mL) at different times after exposure (6, 10, 24 and 30 h), and then, their ability to modulate DNA damage induced by doxorubicin (DOX) at different treatment protocols (pre, post and simultaneous with DOX) and times (12, 24 and 36 h) in mice peritoneal macrophages. In addition, the toxicogenomic potential of citral and eugenol by modulating the expression of NF-KB1, COX-2 and TNF-α (related to inflammatory processes) genes in macrophages activated or not by bacterial lipopolysaccharide (LPS) was also investigated. The results showed that both compounds have genotoxic potential. In the case of citral, genotoxicity was observed for the two major concentrations, but only 6h after the exposure. For eugenol, increased DNA damage was detected for all concentrations, in at least one moment of analysis. Related to the antigenotoxicity, both citral and eugenol presented protective effects at different concentrations and treatment protocols, and the more effective activities were detected at simultaneous and pre-treatment... (Complete abstract click electronic access below)
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5

Silva, Ana Carolina Buzinari da [UNESP]. "Análise de uma biblioteca de mutantes de Xanthomonas citri subsp. citri quanto à patogenicidade." Universidade Estadual Paulista (UNESP), 2014. http://hdl.handle.net/11449/121954.

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O estudo da interação planta-patógeno é de grande importância para o entendimento do cancro cítrico, justificando assim a busca por genes que estejam ligados a patogenicidade e virulência em Xanthomonas citri subsp. citri (Xac), agente causal dessa doença. Neste estudo, foi realizada mutagênese aleatória por inserção do transposon EZ-Tn5 in vitro no genoma da Xac. Obteve-se 8000 mutantes onde 292 foram conduzidos em ensaio experimental in planta. Cinco mutantes expressaram sintomatologia alterada, dois com ausência total de sintomas e três com leve hiperplasia. A análise da sequência dos genes onde se inseriu o transposon indicam mutações nos genes purF, yapH, oar, um gene que codifica uma proteína hipotética (XAC 0196), e na região entre os genes pobB (XAC0362) e glpR (XAC0361). As análises de curvas de crescimento bacteriano in planta demonstraram que, exceto o gene purF, todos os demais podem ser genes envolvidos na patogenicidade de Xac. Dois destes, yapH e oar são descritos como relacionados à adesividade bacteriana, evidenciando que a interferência nesse processo exerce influência direta no sucesso da infecção de Xac. Destaca-se também a importância da identificação de uma proteína hipotética, já que essa apresentou sintomatologia atenuada quando ocorreu a inserção do transposon
The study of plant-pathogen interaction is very important to citrus canker understanding, justifying the search for virulence and pathogenicity related genes in Xanthomonas citri subsp. citri (Xac), causal agent of this disease. In this study, a random mutagenesis by Tn5 transposon insertion into Xac’s genome was performed. Eight thousand mutants were produced and 292 mutants were tested in planta. From those, five mutants expressed altered symptomatology, two showed complete absence of symptoms and three reduced hyperplasia. Gene sequences analysis where transposon was inserted, indicated mutations in purF, yapH and oar genes, in a region that codes for a hypothetical protein (XAC0196), and in a region between pobB (XAC0362) and glpR (XAC0361) genes. Analysis of bacteria growth curve in planta showed that, except for purF gene, all the others genes may be involved in Xac pathogenicity. Two of these genes, yapH and oar, are described as bacterial adhesion related genes, highlighting that interference in this process has direct influence in the Xac infection success. The importance of hypothetical protein identification is emphasized, since it presented attenuated symptomatology when mutated
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Terrazas, Peterson Menezes. "Estudo do potencial genotóxico da Gutiferona A em diferentes células de camundongos in vitro /." Botucatu, 2013. http://hdl.handle.net/11449/108542.

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Orientador: Edson Luis Maistro
Banca: Maria Aparecida Marin Morales
Banca: Cláudia Aparecida Rainho
Resumo: Garcinia achachairu (GAC) é uma planta de origem boliviana que vem sendo utilizada na medicina popular para o tratamento de distúrbios gástricos, reumatismo, inflamações e como cicatrizante. A caracterização fitoquímica do extrato desta planta revelou que, uma benzofenona, a Gutiferona A (GA), é um dos seus compostos majoritários, que segundo estudos recentes, apresenta importante atividade antioxidante e antimicrobiana. Considerando o interesse em se aprofundar as análises do potencial farmacológico da GA e a inexistência de estudos que avaliem a sua toxicidade genética, o presente estudo foi elaborado visando investigar o potencial genotóxico e mutagênico da GA em diferentes células de camundongos in vivo, utilizando alguns dos testes tradicionais na área de mutagênese, como o Ensaio Cometa (EC) para a verificação da genotoxicidade e o Teste do Micronúcleo (TM) para a verificação da mutagenicidade. O experimento foi conduzido com camundongos Suíços albinos machos (Mus musculus) de 12 semanas, divididos em cinco grupos, constituídos cada um por seis animais. O grupo controle negativo recebeu, via gavagem, 0,3 mL de DMSO 1%. O grupo controle positivo, recebeu intraperitonealmente, 80 mg/kg de doxorrubicina. Os grupos tratados receberam, via gavagem, 0,3 mL da GA nas doses de 15, 30 e 60 mg/kg. Para a avaliação da genotoxicidade foi coletado sangue da veia caudal dos camundongos (4 e 24 horas após o tratamento), células do fígado, medula óssea, cérebro e testículos (coletadas 24 horas após o tratamento). Para a avaliação da mutagenicidade, foram coletadas células da medula óssea 24 horas após o tratamento. A citotoxicidade foi avaliada pela contagem de 200 eritrócitos policromáticos (PCE) e normocromáticos (NCE) e determinação de sua razão (PCE/NCE). Na amostra de sangue de 4h, analisadas pelo EC, os resultados obtidos mostraram que nas doses de 30 mg/kg e 60 mg/Kg. A análise ...
Abstract: Garcinia achachairu (GAC) is a native plant from Bolivia that has been used in folk medicine for the treatment of gastric disorders, rheumatism, inflammation and as a healing. The phytochemical characterization of this plant extract revealed that the benzophenone guttiferone A (GA) is one of its major compounds, which according to recent studies, has important antioxidant and antimicrobial activity. Considering the interest in deepening the analysis of the pharmacological potential of GA and the lack of studies assessing its genetic toxicity, the present study was designed in order to investigate the genotoxic and mutagenic effects of GA in different cells of mice in vivo, using some of the traditional tests in the mutagenesis area, the Comet Assay (CA) for genotoxicity evaluation and the Micronucleus Test (MT) for the mutagenicity assessment. The experiment was conducted in Swiss albino male mice (Mus musculus) with 12 weeks, divided into five groups with six animals each. The negative control group received, by oral gavage, 0.3 mL of 1% DMSO. The positive control group received, intraperitoneally, 80 mg/Kg of doxorubicin. The treated groups received 0.3 ml of GA at 15, 30 and 60 mg/kg, by gavage. For the genotoxicity evaluation, blood was collected from the tail vein of the mice (4 and 24 hours after treatment), and liver, bone marrow, brain and testicular cells were collected 24 hours after treatment. For the mutagenicity assessment, bone marrow cells were collected 24 hours after treatment. Cytotoxicity was assessed by scoring 200 consecutive polychromatic (PCE) and normochromatic (NCE) erythrocytes and their ratio (PCE/NCE) determined. For the 4 h blood sample, the results with GA at doses of 30 and 60 mg/kg showed that was a statistically significant increase in DNA damage in comparison to the negative control. For the 24 h blood sample, only 60 mg/kg dose showed significant genotoxicity. The analysis of ther ...
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7

Silva, Ana Carolina Buzinari da. "Análise de uma biblioteca de mutantes de Xanthomonas citri subsp. citri quanto à patogenicidade /." Jaboticabal, 2014. http://hdl.handle.net/11449/121954.

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Orientador: Maria Inês Tiraboschi Ferro
Coorientador: Jesus Aparecido Ferro
Banca: Flavia Maria de Souza Carvalho
Banca: Fabrício José Jaciani
Resumo: O estudo da interação planta-patógeno é de grande importância para o entendimento do cancro cítrico, justificando assim a busca por genes que estejam ligados a patogenicidade e virulência em Xanthomonas citri subsp. citri (Xac), agente causal dessa doença. Neste estudo, foi realizada mutagênese aleatória por inserção do transposon EZ-Tn5 in vitro no genoma da Xac. Obteve-se 8000 mutantes onde 292 foram conduzidos em ensaio experimental in planta. Cinco mutantes expressaram sintomatologia alterada, dois com ausência total de sintomas e três com leve hiperplasia. A análise da sequência dos genes onde se inseriu o transposon indicam mutações nos genes purF, yapH, oar, um gene que codifica uma proteína hipotética (XAC 0196), e na região entre os genes pobB (XAC0362) e glpR (XAC0361). As análises de curvas de crescimento bacteriano in planta demonstraram que, exceto o gene purF, todos os demais podem ser genes envolvidos na patogenicidade de Xac. Dois destes, yapH e oar são descritos como relacionados à adesividade bacteriana, evidenciando que a interferência nesse processo exerce influência direta no sucesso da infecção de Xac. Destaca-se também a importância da identificação de uma proteína hipotética, já que essa apresentou sintomatologia atenuada quando ocorreu a inserção do transposon
Abstract: The study of plant-pathogen interaction is very important to citrus canker understanding, justifying the search for virulence and pathogenicity related genes in Xanthomonas citri subsp. citri (Xac), causal agent of this disease. In this study, a random mutagenesis by Tn5 transposon insertion into Xac's genome was performed. Eight thousand mutants were produced and 292 mutants were tested in planta. From those, five mutants expressed altered symptomatology, two showed complete absence of symptoms and three reduced hyperplasia. Gene sequences analysis where transposon was inserted, indicated mutations in purF, yapH and oar genes, in a region that codes for a hypothetical protein (XAC0196), and in a region between pobB (XAC0362) and glpR (XAC0361) genes. Analysis of bacteria growth curve in planta showed that, except for purF gene, all the others genes may be involved in Xac pathogenicity. Two of these genes, yapH and oar, are described as bacterial adhesion related genes, highlighting that interference in this process has direct influence in the Xac infection success. The importance of hypothetical protein identification is emphasized, since it presented attenuated symptomatology when mutated
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Baeza, Centurión Pablo 1989. "Understanding alternative splicing using deep mutagenesis." Doctoral thesis, Universitat Pompeu Fabra, 2020. http://hdl.handle.net/10803/668749.

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Alternative pre-mRNA splicing is a regulated step in eukaryotic gene expression in which introns are removed from the transcript and exons are joined together to form a mature mRNA. To study the effects of mutations on alternative splicing, we built a mutant library containing all combinations of 12 mutations that accumulated during the emergence of an alternatively-spliced human exon: FAS exon 6. This allowed us to study the effects of individual nucleotide substitutions in thousands of different closely-related genetic contexts. We show that the effect of the same mutation on exon inclusion depends non-monotonically on the inclusion levels of the exon before the mutation is made, with mutations having their strongest splice-altering effects in exons with intermediate levels of inclusion, and their smallest effects in exons that are always skipped or always included. After performing deep mutagenesis in two highly included (constitutive) exons, we find that, in agreement with our previous results, mutations have a very small effect on the inclusion of constitutive exons with the exception of mutations in exon-intron boundaries (splice sites). Since alternative splicing is frequently perturbed in human genetic diseases, we then put these results in a more practical context to address the question of the extent to which random mutations in the human genome are likely to have splice-altering effects. Since most human exons are highly included, we conclude that a random mutation is unlikely to have a splice altering effect, and that altered splicing should only be considered a likely proximal disease mechanism for mutations that affect alternatively spliced exons (included at intermediate levels) or disrupt splice sites.
El empalme alternativo es un proceso de la expresión génica en eucariontes en el que los intrones del transcrito se eliminan, dejando únicamente exones para formar un RNAm maduro. Para estudiar los efectos de mutaciones en este proceso, diseñamos una librería de mutantes con las 12 mutaciones (y todas sus combinaciones) que surgieron a lo largo de la evolución enhumanos de un exón alternativo: el exón 6 de FAS. Esto nos permitió estudiar los efectos de cada mutación en miles de contextos genéticos distintos. Descubrimos que la misma mutación puede tener efectos muy diferentes en el empalme de un exón dependiendo de los niveles de inclusión del mismo. Los mayores efectos se observan en exones con niveles intermedios de inclusión, mientras que los menores efectos ocurren en exones con niveles de inclusión muy altos o muy bajos. Tras mutagenizar dos exones constitutivos, confirmamos que, con la excepción de mutaciones en los sitios de empalme, es poco probable que una mutación afecte la inclusión de dichos exones. Dado que el empalme alternativo es un proceso se encuentra alterado en muchas enfermedades genéticas humanas, pusimos nuestros resultados en un contexto más práctico al plantearnos qué probabilidad hay de que una mutación al azar sea capaz de alterar dicho proceso. Ya que la gran mayoría de exones humanos tienen altos niveles de inclusión, concluimos que es poco probable que una mutación escogida al azar sea capaz de alterar los niveles de inclusión de algún exón. De hecho, esto sólo es probable en el caso de mutaciones en los sitios de empalme o de aquellas que afecten la inclusión de un exón alternativo.
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9

Brown, Jeremy Stuart. "Signature tagged-mutagenesis of aspergillus fumigatus." Thesis, Imperial College London, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.322287.

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Seaman, Jonathan. "Signature-tagged mutagenesis in Rhizobium leguminosarum." Thesis, University of Reading, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.499374.

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Rhizobia are a diverse group of symbiotic alpha-proteobacterial diazotrophs which enter a relationship with specific leguminous plants, in which the plant supplies the bacteria with required compounds whilst the bacteria reduce atmospheric nitrogen into ammonia that the plant uses as a nitrogen source. Modification of rhizobial strains has produced mutants more effective at fixing nitrogen, which in turn results in an increase in biomass of host plants under laboratory conditions but these strains are frequently out competed by wild-type strains in field studies or lost in the intervening years of a crop rotation. This study aimed to establish a library of mutants and a system for screening these strains en masse to identify some of the genes involved in competitive rhizosphere colonization in Rhizobium leguminosam.
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Books on the topic "Mutagenesis"

1

Mutagenesis. New York: TOR, 1993.

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Pruett-Miller, Shondra M., ed. Chromosomal Mutagenesis. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-1862-1.

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Davis, Gregory D., and Kevin J. Kayser, eds. Chromosomal Mutagenesis. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-232-8.

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Pruett-Miller, Shondra M. Chromosomal mutagenesis. New York: Humana Press, 2015.

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Kumar, Nitish, ed. Plant Mutagenesis. Cham: Springer Nature Switzerland, 2024. http://dx.doi.org/10.1007/978-3-031-50729-8.

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D, Davis Gregory, and Kayser Kevin J, eds. Chromosomal mutagenesis. Totowa, N.J: Humana Press, 2008.

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H, Phillips D., and Venitt S, eds. Environmental mutagenesis. Oxford: Bios Scientific Publishers, 1995.

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Reeves, Andrew, ed. In Vitro Mutagenesis. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6472-7.

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Ricke, Steven C., Si Hong Park, and Morgan L. Davis, eds. Microbial Transposon Mutagenesis. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9570-7.

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Mittelman, David, ed. Stress-Induced Mutagenesis. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-6280-4.

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Book chapters on the topic "Mutagenesis"

1

Lázaro, Ester. "Mutagenesis." In Encyclopedia of Astrobiology, 1101–2. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-11274-4_1035.

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Lázaro, Ester. "Mutagenesis." In Encyclopedia of Astrobiology, 1650–51. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-662-44185-5_1035.

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Neuffer, M. G. "Mutagenesis." In The Maize Handbook, 212–19. New York, NY: Springer New York, 1994. http://dx.doi.org/10.1007/978-1-4612-2694-9_23.

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Spencer, John F. T., Dorothy M. Spencer, and I. J. Bruce. "Mutagenesis." In Yeast Genetics, 30–58. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-73356-7_7.

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Crueger, Anneliese. "Mutagenesis." In Biotechnology, 4–45. Weinheim, Germany: Wiley-VCH Verlag GmbH, 2008. http://dx.doi.org/10.1002/9783527620838.ch1.

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Labigne, Agnés, and Peter J. Jenks. "Mutagenesis." In Helicobacter pylori, 335–44. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555818005.ch30.

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Clark, M. S., and W. J. Wall. "Mutagenesis." In Chromosomes, 147–75. Dordrecht: Springer Netherlands, 1996. http://dx.doi.org/10.1007/978-94-009-0073-8_6.

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Lázaro, Ester. "Mutagenesis." In Encyclopedia of Astrobiology, 1. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27833-4_1035-3.

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Lázaro, Ester. "Mutagenesis." In Encyclopedia of Astrobiology, 2036. Berlin, Heidelberg: Springer Berlin Heidelberg, 2023. http://dx.doi.org/10.1007/978-3-662-65093-6_1035.

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Yamane-Ohnuki, Naoko, Kazuya Yamano, and Mitsuo Satoh. "Biallelic Gene Knockouts in Chinese Hamster Ovary Cells." In Chromosomal Mutagenesis, 1–16. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-232-8_1.

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Conference papers on the topic "Mutagenesis"

1

TRICOIRE, LUDOVIC, KEISUKE TSUZUKI, and BERTRAND LAMBOLEZ. "AEQUORIN BIOLUMINESCENCE DISSECTED BY RANDOM MUTAGENESIS." In Chemistry, Biology and Applications. WORLD SCIENTIFIC, 2007. http://dx.doi.org/10.1142/9789812770196_0039.

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Lytle, C. D., P. G. Carney, R. P. Felten, H. F. Bushar, and R. C. Straight. "Mutagenesis of herpesvirus by different photodynamic treatments." In ICALEO® ‘88: Proceedings of the Laser Research in Medicine, Dentistry & Surgery Conference. Laser Institute of America, 1988. http://dx.doi.org/10.2351/1.5057964.

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McDonald, Isabel K., Stephen C. Holmes, Karen J. Young, Joseph S. Vyle, Timothy J. Pickering, and Jane A. Grasby. "Functional group mutagenesis of the hairpin ribozyme." In XIth Symposium on Chemistry of Nucleic Acid Components. Prague: Institute of Organic Chemistry and Biochemistry, Academy of Sciences of the Czech Republic, 1999. http://dx.doi.org/10.1135/css199902306.

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Domingo, Esteban. "LETHAL MUTAGENESIS 2019: A SEQUENCE SPACE ODYSSEY." In Viruses: Discovering Big in Small. TORUS PRESS, 2019. http://dx.doi.org/10.30826/viruses-2019-03.

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Li, Ming. "Highly efficient site-specific mutagenesis in malaria mosquitoes." In 2016 International Congress of Entomology. Entomological Society of America, 2016. http://dx.doi.org/10.1603/ice.2016.115516.

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Wang, Lei, Lisha Kuang, Young-Ok Son, John Andrew Hitron, Pratheeshkumar Poyil, Zhuo Zhang, Jia Luo, Zhigang Wang, and Xianglin Shi. "Abstract 5360: Ethanol enhances arsenic-induced mutagenesis in colon." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-5360.

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Rahmat, Rashida. "Strain Mutagenesis of Stenotrophomonas maltophilia for Higher Exopolysaccharide Production." In IBRAS 2021 INTERNATIONAL CONFERENCE ON BIOLOGICAL RESEARCH AND APPLIED SCIENCE. Juw, 2021. http://dx.doi.org/10.37962/ibras/2021/81-82.

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Yuwei, Dong, Miao Jingzhi, Tang Shirong, Chen Shanglong, and Wu Yonghua. "Chemical Mutagenesis Breeding of Protoplast of Ammonia-oxidizing Bacteria." In 2015 AASRI International Conference on Circuits and Systems (CAS 2015). Paris, France: Atlantis Press, 2015. http://dx.doi.org/10.2991/cas-15.2015.22.

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Zhao, Lihong, and Hongjun Sun. "Breeding of high dye-decolorization strain by UV mutagenesis." In 2011 International Conference on Consumer Electronics, Communications and Networks (CECNet). IEEE, 2011. http://dx.doi.org/10.1109/cecnet.2011.5769338.

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TISI, LAURENCE, CHRISTOPHER LOWE, and JAMES MURRAY. "MUTAGENESIS OF SOLVENT-EXPOSED HYDROPHOBIC RESIDUES IN FIREFLY LUCIFERASE." In Proceedings of the 11th International Symposium. WORLD SCIENTIFIC, 2001. http://dx.doi.org/10.1142/9789812811158_0047.

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Reports on the topic "Mutagenesis"

1

Andrews, Paul W., and Leslie Hill. AS52/GPT Mammalian Mutagenesis Assay. Fort Belvoir, VA: Defense Technical Information Center, May 1996. http://dx.doi.org/10.21236/ada597200.

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Kale, Purushottam. JP8 Induced Mutagenesis and Hormesis. Fort Belvoir, VA: Defense Technical Information Center, March 2008. http://dx.doi.org/10.21236/ada479392.

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Walker, Graham C. Final report [DNA Repair and Mutagenesis - 1999]. Office of Scientific and Technical Information (OSTI), May 2001. http://dx.doi.org/10.2172/807345.

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Eaton-Rye, Dr., Julian, and Gaozhong Shen. Specific mutagenesis of a chlorophyll-binding protein. Progress report. Office of Scientific and Technical Information (OSTI), January 1990. http://dx.doi.org/10.2172/5701773.

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Sun, LuZhe. Effect of Estrogen on Mutagenesis in Human Mammary Epithelial Cells. Fort Belvoir, VA: Defense Technical Information Center, June 2005. http://dx.doi.org/10.21236/ada443767.

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Thilly, W. G. Comparative mutagenesis of human cells in vivo and in vitro. Office of Scientific and Technical Information (OSTI), May 1992. http://dx.doi.org/10.2172/10152396.

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Author, Not Given. Analysis of cyanobacterial photosystem 2 genes by cloning and mutagenesis. Office of Scientific and Technical Information (OSTI), January 1989. http://dx.doi.org/10.2172/5079285.

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Thilly, W. G. (Comparative) mutagenesis of human cells in vivo and in vitro. Office of Scientific and Technical Information (OSTI), January 1989. http://dx.doi.org/10.2172/7235709.

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Thilly, W. G. Comparative mutagenesis of human cells in vivo and in vitro. Office of Scientific and Technical Information (OSTI), January 1990. http://dx.doi.org/10.2172/7279262.

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Thilly, W. G. Comparative mutagenesis of human cells in vivo and in vitro. Office of Scientific and Technical Information (OSTI), May 1992. http://dx.doi.org/10.2172/5115937.

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