La historia socioeconómica ecuatoriana del siglo XVIII: análisis y tendencias

This article offers exhaustive, descriptive and critical bibliographical information, full of suggestions, with a view to guiding research into the social and economic history of Ecuador in the eighteenth century. Speical attention in paid to existing general studies, the mining sector, farming, textiles, trade, demography and urban growth, elites, and the impact of bourbon reforms.Este artículo ofrece una información critico-bibliográfica exhaustiva, descriptiva y llena de sugerencias, cuyo objetivo estriba en orientar el desarrollo de investigaciones sobre la historia socio-económica del Ecuador durante el siglo XVIII. Los autores fijan su atención en los aspectos siguientes: estudios generales existentes, el sector minero, el agrario, las manufacturas textiles, el comercio, la demografía y el desarrollo urbano, las élites y la incidencia de las reformas borbónicas

Non-recombinogenic roles for Rad52 in translesion synthesis during DNA damage tolerance

Resumen del trabajo presentado en el Chromatin dynamics and nuclear organization in genome maintenance - EMBO workshop (2020), celebrado de forma virtual del 7 al 10 de diciembre de 2020DNA damage tolerance relies on homologous recombination (HR) and translesion synthesis (TLS) mechanisms to fill in the ssDNA gaps generated during the replication fork bypass of blocking DNA lesions. Whereas TLS requires specialized polymerases able to incorporate a dNTP opposite the lesion and is error-prone, HR uses the sister chromatid to repair the ssDNA gap and is mostly error-free. We report that the HR protein Rad52 acts in concert with the TLS machinery (Rad6/Rad18-mediated PCNA ubiquitylation and polymerases Rev1/Pol ¿) to repair ssDNA gaps through a nonrecombinogenic function, and accordingly Rad52 is required for DNA damage-induced mutagenesis. Specifically, the early HR proteins Rad52, Rad51 and Rad57, but not Rad54, facilitate Rad6/Rad18 binding to chromatin and subsequent DNA damageinduced PCNA ubiquitylation. In sum, Rad51, Rad52 and Rad57 drive the tolerance process to HR or TLS through recombinational and non-recombinational functions, providing a novel role for the recombination proteins in maintaining genome integrity.Peer reviewe

Non-recombinogenic roles for Rad52 in translesion synthesis during DNA damage tolerance

DNA damage tolerance relies on homologous recombination (HR) and translesion synthesis (TLS) mechanisms to fill in the ssDNA gaps generated during passing of the replication fork over DNA lesions in the template. Whereas TLS requires specialized polymerases able to incorporate a dNTP opposite the lesion and is error-prone, HR uses the sister chromatid and is mostly error-free. We report that the HR protein Rad52-but not Rad51 and Rad57-acts in concert with the TLS machinery (Rad6/Rad18-mediated PCNA ubiquitylation and polymerases Rev1/Pol ¿) to repair MMS and UV light-induced ssDNA gaps through a non-recombinogenic mechanism, as inferred from the different phenotypes displayed in the absence of Rad52 and Rad54 (essential for MMS- and UV-induced HR); accordingly, Rad52 is required for efficient DNA damage-induced mutagenesis. In addition, Rad52, Rad51, and Rad57, but not Rad54, facilitate Rad6/Rad18 binding to chromatin and subsequent DNA damage-induced PCNA ubiquitylation. Therefore, Rad52 facilitates the tolerance process not only by HR but also by TLS through Rad51/Rad57-dependent and -independent processes, providing a novel role for the recombination proteins in maintaining genome integrity.Spanish Government. Grant Numbers: BFU2015‐63698‐P, PGC2018‐099182‐B‐I00, BFU2015‐65417‐R, RTI2018‐099055‐B‐I00, BFU2015‐69142‐REDT European Research Council. Grant Number: ERC AdG323179 Marie Sklodowska‐Curie Fellowship. Grant Number: MSCA‐IF‐2017‐79405