Capítulos (Genética)

URI permanente para esta colecciónhttps://hdl.handle.net/11441/10880

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DNA Methylation in Prokaryotes
(Springer Nature, 2022) Casadesús Pursals, Josep; Sánchez Romero, María Antonia; Universidad de Sevilla. Departamento de Genética; Universidad de Sevilla. Departamento de Microbiología y Parasitología; Ministerio de Ciencia e Innovación (MICIN). España
he genomes of bacteria, archaea, and phage contain small amounts of C5-methylcytosine, N4-methylcytosine, and N6-methyladenine. Base methylation takes place after DNA replication and is catalyzed by DNA methyltransferases that recognize specific target sequences. Prokaryotic DNA methyltransferases can be classified into two main types: (1) belonging to restriction-modification systems and (2) solitary (or “orphan”) enzymes that lack a restriction enzyme partner. All known roles of DNA methylation involve control of interactions between DNA-binding proteins and their cognate sites. Such roles include protection from DNA restriction, strand discrimination during mismatch repair, cell cycle control, and regulation of transcription. DNA methylation often affects the interaction of bacterial pathogens with their hosts, raising the possibility of epigenetic therapies for infectious diseases.
Coupling Between Messenger RNA Synthesis and Degradation during Genome Expression
(Fidetia, 2015) Chávez de Diego, Sebastián; Pérez Aguado, David; Chávez de Diego, María José; Romero Campero, Francisco José; Universidad de Sevilla. Departamento de Genética; Universidad de Sevilla. Departamento de Matemática Aplicada I (ETSII); Universidad de Sevilla. Departamento de Ciencias de la Computación e Inteligencia Artificial; Junta de Andalucía
Genome expression involves the synthesis of messenger RNA (mRNA), a short lived molecule whose translation directs the synthesis of cellular proteins and that is subject to degradation after the translation process. Up to the date, mRNA synthesis and degradation has been considered as a linear phenomenon in which the above steps occur subsequently without a regulatory interconnection. However, gene expression can be studied as a global system in which all their stages are coupled and interconnected by regulatory mechanisms. We have contributed to demonstrate that the machineries of mRNA synthesis and degradation physically and functionally interact in the cell nucleus. We have proposed that it allows the cross-regulation of transcription with mRNA degradation and vice versa, giving rise to a circular system, which would explain the large robustness observed in gene expression (Haimovich et al, 2013).
Bacterias buenas o malas: un proyecto para la concientizacion de ninos de primaria sobre la higienizacion en tiempos de pandemia.
(Dykinson, 2023) Piubeli, Francine; Piubeli Doro, João Lucas; Universidad de Sevilla. Departamento de Genética
Aprendiendo con el Scratch: Un proyecto de Innovación docente para fomentar el pensamiento computacional
(Dykinson, 2023) Piubeli, Francine; Piubeli Doro, João Lucas; Universidad de Sevilla. Departamento de Genética
Innovación docente en las prácticas de laboratorio de genética: clase invertida y pensamiento crítico
(Dykinson, 2023) Castellano Pozo, Maikel; Iglesias Sigüenza, Francisco Javier; Comaills, Valentine; Valle Rosado, Iván; Universidad de Sevilla. Departamento de Biología Celular; Universidad de Sevilla. Departamento de Genética; Universidad de Sevilla. Departamento de Química orgánica
Un ciclo de mejora docente para estudiar Evolución Molecular
(Universidad de Sevilla, 2022) Jimeno González, Silvia; Universidad de Sevilla. Departamento de Genética
En asignaturas de genética, aprender a resolver problemas es esencial para fortalecer la integración de los conceptos que se imparten en las clases teóricas. De hecho, el modelo metodológico tradicional suele basarse en la exposición teórica en clase y la resolución de dichos problemas como trabajo para casa. En este capítulo, se describe el diseño y la aplicación de un ciclo de mejora en el aula para el tema de Evolución Molecular de la asignatura Genética Molecular del Grado de Biomedicina básica y experimental, que tiene como objetivo aumentar la participación del alumno en el proceso de enseñanza-aprendizaje. Para ello, la resolución de problemas se intercala dentro de la dinámica de la clase, llevándose a cabo tanto de forma individual como en pequeños grupos. Por otro lado, algunas de las actividades inicialmente propuestas se han adaptado al resultado del cuestionario de ideas previas de los alumnos para poder construir sobre ellas o trabajar conceptos preconcebidos erróneos. Los resultados de las escaleras de aprendizaje muestran un incremento considerable en los conocimientos de los alumnos al término de la unidad didáctica. Por otro lado, la respuesta de los estudiantes ha sido ciertamente positiva, expresada tanto a nivel personal como en las calificaciones del examen parcial correspondiente.
Biosíntesis de carotenoides en hongos
(Terracota, 2017) Ávalos Cordero, Francisco Javier; Limón Mirón, María del Carmen; Universidad de Sevilla. Departamento de Genética
The Sister-Chromatid Exchange Assay in Human Cells
(Humana, 2020) Tumini, Emanuela; Aguilera López, Andrés; Universidad de Sevilla. Departamento de Genética
The semiconservative nature of DNA replication allows the differential labeling of sister chromatids that isthe fundamental requirement to perform the sister-chromatid exchange (SCE) assay. SCE assay is apowerful technique to visually detect the physical exchange of DNA between sister chromatids. SCEscould result as a consequence of DNA damage repair by homologous recombination (HR) during DNAreplication. Here, we provide the detailed protocol to perform the SCE assay in cultured human cells. Cellsare exposed to the thymidine analog 5-bromo-20-deoxyuridine (BrdU) during two cell cycles, resulting inthe two sister chromatids having differential incorporation of the analog. After metaphase spreads prepara-tion and further processing, SCEs are nicely visualized under the microscope.
Detection of DNA Double-Strand Breaks byγ-H2AX Immunodetection
(Humana, 2020) Barroso, Sonia I.; Aguilera López, Andrés; Universidad de Sevilla. Departamento de Genética
DNA double-strand breaks (DSBs) are the most deleterious type of DNA damage and a cause of geneticinstability as they can lead to mutations, genome rearrangements, or loss of genetic material when notproperly repaired. Eukaryotes from budding yeast to mammalian cells respond to the formation of DSBswith the immediate phosphorylation of a histone H2A isoform. The modified histone, phosphorylated inserine 139 in mammals (S129 in yeast), is namedγ-H2AX. Detection of DSBs is of high relevance inresearch on DNA repair, aging, tumorigenesis, and cancer drug development, given the tight association ofDSBs with different diseases and its potential to kill cells. DSB levels can be obtained by measuring levels ofγ-H2AX in extracts of cell populations or by counting foci in individual nuclei. In this chapter sometechniques to detectγ-H2AX are described.
The rem mutations in the ATP-binding groove of the Rad3/XPD helicase lead to Xeroderma pigmentosum-Cockayne Syndrome-like phenotypes
(Public Library of Science, 2014) Herrera Moyano, Emilia; Moriel Carretero, María; Montelone, Beth A.; Aguilera López, Andrés; Universidad de Sevilla. Departamento de Genética
The eukaryotic TFIIH complex is involved in Nucleotide Excision Repair and transcription initiation. We analyzed three yeast mutations of the Rad3/XPD helicase of TFIIH known as rem (recombination and mutation phenotypes). We found that, in these mutants, incomplete NER reactions lead to replication fork breaking and the subsequent engagement of the homologous recombination machinery to restore them. Nevertheless, the penetrance varies among mutants, giving rise to a phenotype gradient. Interestingly, the mutations analyzed reside at the ATP-binding groove of Rad3 and in vivo experiments reveal a gain of DNA affinity upon damage of the mutant Rad3 proteins. Since mutations at the ATP-binding groove of XPD in humans are present in the Xeroderma pigmentosum-Cockayne Syndrome (XP-CS), we recreated rem mutations in human cells, and found that these are XP-CS-like. We propose that the balance between the loss of helicase activity and the gain of DNA affinity controls the capacity of TFIIH to open DNA during NER, and its persistence at both DNA lesions and promoters. This conditions NER efficiency and transcription resumption after damage, which in human cells would explain the XP-CS phenotype, opening new perspectives to understand the molecular basis of the role of XPD in human disease.

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