Revista de Vertebrados de la Estación Biológica de Doñana

Página 298 con error de impresiónEstudio cariológico en dos especies de Serránidos del Mediterráneo (Peces: PerciformesRelaciones morfométricas de Atherina boyeri Risso (Pisces: Atherinidae) de la laguna de Zoñar (Córdoba, España)Contribución al conocimiento de la biometríay osteología de Barbus barbus bocagei, Steindachner, 1866 (Pisces: CyprinidaeLa actividad de la salamandra, Salamandra salamandra (L.), en Galicia.Estudios sobre el sapo corredor (Bufo calamita) en el Sur de España.1. BiometríaEstudios sobre el sapo corredor (Bufo calamita) en el Sur de España. II. AlimentaciónBiología de la reproducción de Rana iberica Boulenger 1879 en zonas simpátridas con Rana temporaria Linneo, 1758Nuevos datos sobre la distribución geográfica de Lacerta monticola cantabrica Mertens, 1929. (Sauria, lacertidae).Datos sobre Lacerta monticola Boulenger, 1905 (Saurio: lacertidae)en el oeste del Sistema Central.Nueva especie de Anolis (lacertilia, Iguanidae) para CubaEtograma cuantificado del cortejo en Falco naumannOntogénesis del comportamiento predador en Falco naumanniContaminación xenobiótica del Parque Nacional de Doñana. 1. Residuos de insecticidas organoclorados, bifenilos policlorados y mercurio en anseriformes y gruiformesReproducción del críalo (Clamator glandarius) en Sierra Morena CentraNidificación de Picus viridis en taludes de arcilla en Ramblas de Guadix (Granada)Comportamiento del calamón Porphyrio porphyrio (Linnaeus, 1758) en Doñana, Marismas del GuadalquiviBiología y ecología de la malvasía (Oxyura leucocephala) en Andalucía.On the differential diet of Carnivora in islands:a method for analysing it and a particular case.Notas sobre la distribución pasada y actual del meloncillo Herpestes ichneumon (L.) en la Península IbéricaEstructuración de las interacciones en una camada de lobos (Canís lupus)Nuevos datos sobre la distribución del Cottus gobio L. (pisces, cottidae) en EspañaSobre la alimentación de Callopistes maculatus (Reptilia,teiidaeObservación de Lacerta lepida depredando un nido de Alectoris rufaNueva cita del galápago leproso Mauremys leprosa (Scheigger, 1812) en los pirineosPrimera cita de Psammodromus hispanicus (Fitzinger) para GaliciaSobre la presencia de Gallotia (=Lacerta) atlantica (Peters y Doria, 1882) en Gran CanariaNota sobre las Lacerta monticola Boulenger, 1905 de las zonas del norte de GaliciaPrimeras notas herpetológicas de la provincia de Soria.Datos sobre selección de hábitat y ecología alimenticia del porrón pardo (Aythya nyroca)Probable nueva área de cría del pechiazul (Luscinia svecica cyanecula) en el sistema central. PerisPredación de Falco peregrinus y Falco subbuteo sobre quirópterosResultados de la producción de Oxyura leucocephala en el año 1981 en las lagunas de Zóñar y el rincónAnálisis de la dieta de Tyto alba en un medio árido antropógeno de los alrededores de Almería¿Son Eudocimus ruber y E. albus distintas especies?EL Estornino pinto (Sturnus vulgaris) en Canarias: nueva especie nidifiante en el archipiélagoDatos sobre la alimentación otoñal del cárabo (Strix aluco) en la sierra de CádizObservación primaveral de rapaces y otras aves en el páramo del estado de Mérida (Venezuela).Murciélago hematófago (Desmodus rotundus) parasitando a un chigüire (Hidrochoerus hydrochaeris)Observaciones sobre la reproducción del zacatuche o teporinho Romerolagus diazi (Mammalia: lagomorpha)Estudio electroforético de hemoglobinas y esterasas sanguíneas en Rhinolophus ferrumequinum (Chiroptera: rhinolophidae) y de hemoglobinas en Tadaria taeniotis (chiroptera: molossidae)Peer reviewe

Mapping density, diversity and species-richness of the Amazon tree flora

Using 2.046 botanically-inventoried tree plots across the largest tropical forest on Earth, we mapped tree species-diversity and tree species-richness at 0.1-degree resolution, and investigated drivers for diversity and richness. Using only location, stratified by forest type, as predictor, our spatial model, to the best of our knowledge, provides the most accurate map of tree diversity in Amazonia to date, explaining approximately 70% of the tree diversity and species-richness. Large soil-forest combinations determine a significant percentage of the variation in tree species-richness and tree alpha-diversity in Amazonian forest-plots. We suggest that the size and fragmentation of these systems drive their large-scale diversity patterns and hence local diversity. A model not using location but cumulative water deficit, tree density, and temperature seasonality explains 47% of the tree species-richness in the terra-firme forest in Amazonia. Over large areas across Amazonia, residuals of this relationship are small and poorly spatially structured, suggesting that much of the residual variation may be local. The Guyana Shield area has consistently negative residuals, showing that this area has lower tree species-richness than expected by our models. We provide extensive plot meta-data, including tree density, tree alpha-diversity and tree species-richness results and gridded maps at 0.1-degree resolution

Mapping density, diversity and species-richness of the Amazon tree flora

Using 2.046 botanically-inventoried tree plots across the largest tropical forest on Earth, we mapped tree species-diversity and tree species-richness at 0.1-degree resolution, and investigated drivers for diversity and richness. Using only location, stratified by forest type, as predictor, our spatial model, to the best of our knowledge, provides the most accurate map of tree diversity in Amazonia to date, explaining approximately 70% of the tree diversity and species-richness. Large soil-forest combinations determine a significant percentage of the variation in tree species-richness and tree alpha-diversity in Amazonian forest-plots. We suggest that the size and fragmentation of these systems drive their large-scale diversity patterns and hence local diversity. A model not using location but cumulative water deficit, tree density, and temperature seasonality explains 47% of the tree species-richness in the terra-firme forest in Amazonia. Over large areas across Amazonia, residuals of this relationship are small and poorly spatially structured, suggesting that much of the residual variation may be local. The Guyana Shield area has consistently negative residuals, showing that this area has lower tree species-richness than expected by our models. We provide extensive plot meta-data, including tree density, tree alpha-diversity and tree species-richness results and gridded maps at 0.1-degree resolution

Regulación de la rutas de tolerancia a daños replicativos dependientes de RAD6, RAD5 y RAD52 durante el ciclo celular en Saccharomyces cerevisiae

Trabajo realizado en el Departamento de Genética, Facultad de Biología, Universidad de Sevilla y en el Departamento de Biología de Genomas, CABIMER, para optar al grado de Doctor en Biología.--Calificación: Sobresaliente cum laudeLa tolerancia al daño en el ADN se basa en los mecanismos de recombinación homóloga (HR) y de síntesis translesión (TLS) para completar post-replicativamente las lesiones de ssDNA generadas durante el bypass de la horquilla de replicación. Mientras que TLS requiere polimerasas especializadas capaces de incorporar un dNTP opuesto a la lesión y es propenso a errores, HR usa la cromatida hermana para reparar las lesiones de ssDNA y en su mayoría está libre de errores. En este trabajo se demuestra que las proteínas de HR Rad52, Rad51 y Rad57 colaboran con la maquinaria de TLS (ubiquitinación de PCNA mediada por Rad6/Rad18 y las polimerasas Rev1/Pol z) para reparar las lesiones de ssDNA a través de una función no recombinogénica, y en consecuencia son necesarias para la mutagénesis inducida por daño en el ADN. Específicamente, se requieren Rad52, Rad51 y Rad57, pero no Rad54, para la unión de Rad6/Rad18 a la cromatina y la subsiguiente ubiquitinación de PCNA inducida por daños en el ADN. En resumen, Rad51, Rad52 y Rad57 dirigen el proceso de tolerancia a HR o TLS a través de funciones recombinogénicas y no recombinogénicas, proporcionando un nuevo papel para las proteínas de recombinación en el mantenimiento de la integridad del genoma

A mechanism for the recruitment of recombination proteins during DNA damage tolerance

Resumen del póster presentado al XXXIX Congreso de la Sociedad Española de Bioquímica y Biología Molecular, celebrado en Salamanca del 5 al 8 de septiembre de 2016.The recombination proteins Rad52 and Rad51 help the fork to pass through blocking lesions and to fill in the gaps of ssDNA generated during the process of lesion bypass. Their recruitment to the ssDNA lesions has obligatorily to occur during S phase. Here we show that Rad52 and Rad51 display the same kinetics of chromatin binding as the helicase Mcm2-7: they accumulate in G1, are released during replication, and remain bound to chromatin in the presence of replicative blocking lesions. This coordinated response requires Cdc7-dependent physical interactions between Rad51/Rad52 and the Mcm2-7 helicases that are not at the fork. Accordingly, reducing Cdc7 activity impairs sister-chromatid junction formation and ssDNA filling by recombination. Therefore, the loading of Rad51 and Rad52 in G1, together with a Mcm2-7-mediated mechanism that couples the fork advance with Rad52/Rad51 binding to replicative damage, provides a strategy to ensure the filling of the ssDNA lesions through an error-free repair mechanism.Peer reviewe

Cdc7-dependent interactions of Mcm2-7 with G1-loaded Rad51 and Rad52 regulate the recombinational response to replicative damage

Resumen del póster presentado a la Conferencia Mechanisms of Recombination, celebrada en Alicante (España) del 16 al 20 de mayo de 2016.The response to DNA lesions that impair the advance of replication forks relies on DNA damage tolerance (DDT) mechanisms, which facilitate fork bypass across the lesions and repair of the ssDNA fragments generated during this process. One of these mechanisms is Homologous Recombination (HR), which uses the information of an intact template to repair the ssDNA fragments. An important mechanistic difference with the replication-independent process of double-strand break (DSB) repair by HR is that Rad52 and Rad51 travel with the forks and their loading into the ssDNA lesions is coupled to DNA replication. We show in Saccharomyces cerevisiae that Rad51 interacts physically with the replicative helicase MCM2-7 regardless of the presence of DNA damage, and that this interaction requires the continuous activity during S phase of the cell-cycle master kinase Cdc7. Remarkably, even though Rad51 and MCM2-7 are recruited independently to chromatin, they display similar kinetics of DNA binding during the cell cycle. In the absence of DNA damage they accumulate in G1 and are released as replication is completed, whereas in the presence of the alkylating agent methyl-methane sulfonate (MMS) they remain bound to chromatin, suggesting that the helicase MCM2-7 plays a role in DDT. The loading/stabilization of Rad51 in response to MMS requires the kinase activity of Cdc7. Likewise, the binding of Rad52 to ssDNA lesions generated upon treatment with MMS is impaired in a thermosensitive cdc7-4 allele at semi-permissive temperature, being this effect independent of the roles of Cdc7 on replication initiation, checkpoint activation or translesion synthesis. Instead, it is partially mediated by phosphorylation of Mcm2 at serines 164 and 170. However, neither cdc7-4 nor a phosphomimetic mcm2AA affect the association between Rad51 and MCM2-7, suggesting that Cdc7 maintains Rad52/Rad51/MCM2-7 at chromatin in response to DNA damage through a different mechanism. Consistent with these results a reduction in the kinase activity of Cdc7 affects the kinetics of sister-chromatid junctions and Rad52 repair in response to MMS. Overall, these results uncover a novel role for Cdc7 in the recombinational branch of DDT by regulating the binding of Rad51 to chromatin in coordination with the helicase MCM2-7.Peer Reviewe

Rad51 and Rad52 supply to replicative DNA lesions relies on cell cycle regulated interactions with the Mcm2-7 helicase

Resumen del póster presentado a la EMBO Conference: The DNA damage response in cell physiology and disease, celebrada en Atenas (Grecia) del 2 al 6 de octubre de 2017.The recombination proteins Rad51 and Rad52 help the fork to bypass blocking lesions and fill in the gaps of ssDNA generated during this process of DNA damage tolerance (DDT). Their recruitment to the ssDNA lesions must occur during S phase. Here we show that Rad51, Rad52 and the Mcm2-7 helicase display similar patterns of chromatin binding: they accumulate in G1, are released during replication and remain bound to chromatin in the presence of replicative blocking lesions. Moreover, their binding to chromatin during S phase requires the kinase activity of Cdc7. This kinetics of chromatin binding is coordinated through physical interactions between Rad51 and Rad52 with Mcm2-7. These interactions are prevented at the pre-replication complex and at the replication fork, suggesting that they occur with the excess of Mcm2-7 helicases that are loaded in G1. Importantly, Cdc7-mediated Mcm2-7/Rad51/Rad52 accumulation at chromatin is required for ssDNA filling by recombination, supporting the relevance of these interactions and providing new functions for Cdc7 in DDT. We propose that chromatin recruitment of Rad51/Rad52 in G1, together with a mechanism mediated by Mcm2-7 to supply Rad51/Rad52 to replicative ssDNA lesions, provide a strategy for ensuring that ssDNA lesions are filled via an error-free repair mechanism.Peer Reviewe

Physical interactions of Rad51 and Rad52 with Mcm2-7 coordinate their binding to chromatin during the cell cycle and In response to DNA damage

Resumen del póster presentado a la 28th International Conference on Yeast Genetics and Molecular Biology (ICYGMB), celebrada en Praga (Czech Republic) del 27 de agosto al 1 de septiembre de 2017.The recombination proteins Rad51 and Rad52 help the fork to bypass blocking lesions and fill in the gaps of single-stranded DNA (ssDNA) generated during this process of DNA damage tolerance (DDT). In contrast to DNA double-strand breaks, Rad51 and Rad52 recruitment to the ssDNA lesions must occur during S phase. Here we show that Rad51 and Rad52 physically interact with the replicative helicase Mcm2-7 in G1. These interactions are lost during replication unless cells divide in the presence of replicative blocking lesions. They occur mostly in chromatin but are prevented at the pre-RC and at the replication forks, suggesting that Rad51 and Rad52 interact with the excess of Mcm2-7 helicases loaded in G1 and spread to the vicinity of the replication origins. Indeed, Mcm2-7 and Rad51 accumulate at a nuclease-insoluble chromatin fraction enriched in replication factors. Notably, these interactions coordinate the kinetics of chromatin binding of Mcm2-7, Rad51 and Rad52, which accumulate in G1, are released during S/G2 and are maintained in the presence of replicative DNA damage. This chromatin binding behavior is remarkable because homologous recombination is inactive in G1 and active during S/G2. Interestingly, the kinase activity of Cdc7 is required to preserve both the integrity of the Mcm2-7/Rad51/Rad52 complexes and the presence of these factors at chromatin during S/G2. Our results suggest novel roles for Cdc7 and Mcm2-7 in the regulation of the location of recombination proteins during DDT.Peer Reviewe

Non-recombinogenic role for Rad52, Rad51 and Rad57 in translesion synthesis

Resumen del trabajo presentado en el 1st CABIMER International Workshop Trends in Genome Integrity & Chromosome Dynamics, celebrado en Sevilla (España), del 19 al 21 de febrero 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 non-recombinogenic 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 damage-induced 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

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