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Zim17/Tim15 links mitochondrial iron–sulfur cluster biosynthesis to nuclear genome stability

Opened Access Zim17/Tim15 links mitochondrial iron–sulfur cluster biosynthesis to nuclear genome stability

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Autor: Díaz de la Loza, María del Carmen
Gallardo Ortega, Mercedes
García Rubio, María Luisa
Izquierdo, Alicia
Herrero, Enrique
Aguilera López, Andrés
Wellinger, Ralf Erik
Departamento: Universidad de Sevilla. Departamento de Genética
Fecha: 2011
Publicado en: Nucleic Acids Research, 39 (14), 6002-6015.
Tipo de documento: Artículo
Resumen: Genomic instability is related to a wide-range of human diseases. Here, we show that mitochondrial iron–sulfur cluster biosynthesis is important for the maintenance of nuclear genome stability in Saccharomyces cerevisiae. Cells lacking the mitochondrial chaperone Zim17 (Tim15/Hep1), a component of the iron–sulfur biosynthesis machinery, have limited respiration activity, mimic the metabolic response to iron starvation and suffer a dramatic increase in nuclear genome recombination. Increased oxidative damage or deficient DNA repair do not account for the observed genomic hyperrecombination. Impaired cell-cycle progression and genetic interactions of ZIM17 with components of the RFC-like complex involved in mitotic checkpoints indicate that replicative stress causes hyperrecombination in zim17Δ mutants. Furthermore, nuclear accumulation of pre-ribosomal particles in zim17Δ mutants reinforces the importance of iron–sulfur clusters in normal ribosome biosynthesis. We propose that compromi...
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Cita: Díaz de la Loza, M.d.C., Gallardo Ortega, M., García Rubio, M.L., Izquierdo, A., Herrero, E., Aguilera López, A. y Wellinger, R.E. (2011). Zim17/Tim15 links mitochondrial iron–sulfur cluster biosynthesis to nuclear genome stability. Nucleic Acids Research, 39 (14), 6002-6015.
Tamaño: 6.641Mb
Formato: PDF

URI: https://hdl.handle.net/11441/71202

DOI: 10.1093/nar/gkr193

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