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Félix Prado

Researcher at University of Seville

Publications -  41
Citations -  1772

Félix Prado is an academic researcher from University of Seville. The author has contributed to research in topics: Homologous recombination & Chromatin. The author has an hindex of 18, co-authored 37 publications receiving 1614 citations. Previous affiliations of Félix Prado include Spanish National Research Council.

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Impairment of replication fork progression mediates RNA polII transcription-associated recombination

TL;DR: This work provides evidence that one mechanism responsible for TAR is RNAP‐mediated replication impairment, and using novel plasmid‐borne recombination constructs in Saccharomyces cerevisiae shows that RNA polymerase II (RNAPII) transcription induces recombination by impairing replication fork progression.
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Replication fork progression is impaired by transcription in hyperrecombinant yeast cells lacking a functional THO complex.

TL;DR: Evidence that deficient mRNP biogenesis causes slowdown or pausing of the replication fork in hpr1Δ mutants is provided and transcription-dependent genomic instability in THO mutants with impaired replication fork progression is linked, suggesting a molecular basis for a connection between inefficient mR NP biogenesis and genetic instability.
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Role of reciprocal exchange, one-ended invasion crossover and single-strand annealing on inverted and direct repeat recombination in yeast: different requirements for the RAD1, RAD10, and RAD52 genes.

TL;DR: It is proposed that deletions can occur as three types of recombination events: the conservative RAD52-dependent reciprocal exchange and the nonconservative events, one-ended invasion crossover, and single-strand annealing (SSA).
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Hpr1 is preferentially required for transcription of either long or G+C-rich DNA sequences in Saccharomyces cerevisiae.

TL;DR: It is demonstrated that Hpr1 is a factor required for transcription of long as well as G+C-rich DNA sequences, and both length and G-C content are important elements influencing transcription in vivo.
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The SWR1 Histone Replacement Complex Causes Genetic Instability and Genome-Wide Transcription Misregulation in the Absence of H2A.Z

TL;DR: The results support a stepwise mechanism for the replacement of H2A with Htz1 and demonstrate that a tight control of this mechanism is essential to regulate chromatin dynamics but also to prevent the deleterious consequences of an incomplete nucleosome remodelling.