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© 2018 Amo et al., Small birds use cavities for roosting to decrease the thermoregulatory costs during the winter nights. The ability of birds to detect and escape from an approaching predator is impaired during roosting and thus the selection of such cavities should take into account the risk that a predator will find the cavity. Previous evidence suggested that birds in captivity are able to detect predator scent and avoid roosting in nest-boxes containing such predator chemical cues. Here, we tested whether birds also show this avoidance response under natural conditions. We performed three studies in three populations of blue and great tits. We added predator scent, a pungency scent or an odourless control to nest-boxes and compared the use of these nest-boxes for roosting. We found no differences between the scent treatments in the use of nest-boxes. Therefore, chemical cues indicating the potential presence of a predator are not enough for birds to avoid roosting in nest-boxes under natural conditions., L.A. and G.T. were supported by the postdoctoral JAE-CSIC, the postdoctoral MEC and by the Ramon y Cajal program. IRG was supported by the predoctoral FPI program. The study was funded by the MINECO project CGL2014-58890-P to L.A. and G.T.

This is an openaccess article distributed under the terms of the Creative Commons Attribution License.-- et al., The Shoc2 protein has been implicated in the positive regulation of the Ras-ERK pathway by increasing the functional binding interaction between Ras and Raf, leading to increased ERK activity. Here we found that Shoc2 overexpression induced sustained ERK phosphorylation, notably in the case of EGF stimulation, and Shoc2 knockdown inhibited ERK activation. We demonstrate that ectopic overexpression of human Shoc2 in PC12 cells significantly promotes neurite extension in the presence of EGF, a stimulus that induces proliferation rather than differentiation in these cells. Finally, Shoc2 depletion reduces both NGF-induced neurite outgrowth and ERK activation in PC12 cells. Our data indicate that Shoc2 is essential to modulate the Ras-ERK signaling outcome in cell differentiation processes involved in neurite outgrowth., GL, TG and LMD were recipients of fellowships from the Ministerio de Educación y Ciencia (MEC) (to GL, TG), and Fondo de Investigaciones Sanitarias (FIS) (to LMD). LSR held a postdoctoral research contract from CIBERNED. This work was supported by FIS grant (PI10/00815) to JLO; CIBERNED to MC; SAF2008-01951, Comunidad Autónoma de Madrid (CAM) SSAL-0202-2006-01 and Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED) to TI; FIS grant PI12/00775 and ISCIII-RETIC (Red Temática de Investigación Cooperativa en Cáncer) RD12/0036/0027 from the Instituto de Salud Carlos III to PSG; and FIS grants (PI09/0562 and PI13/00703), ISCIIIRETIC (RD06/0020/0003 and RD12/0036/0021), and the Spanish Association Against Cancer (AECC) to JMR.

© 2014 Gomila et al. The Achromobacter is a genus in the family Alcaligenaceae, comprising fifteen species isolated from different sources, including clinical samples. The ability to detect and correctly identify Achromobacter species, particularly A. xylosoxidans, and differentiate them from other phenotypically similar and genotypically related Gram-negative, aerobic, non-fermenting species is important for patients with cystic fibrosis (CF), as well as for nosocomial and other opportunistic infections. Traditional phenotypic profile-based analyses have been demonstrated to be inadequate for reliable identifications of isolates of Achromobacter species and genotypic-based assays, relying upon comparative 16S rRNA gene sequence analyses are not able to insure definitive identifications of Achromobacter species, due to the inherently conserved nature of the gene. The uses of alternative methodologies to enable high-resolution differentiation between the species in the genus are needed. A comparative multi-locus sequence analysis (MLSA) of four selected 'house-keeping' genes (atpD, gyrB, recA, and rpoB) assessed the individual gene sequences for their potential in developing a reliable, rapid and cost-effective diagnostic protocol for Achromobacter species identifications. The analysis of the type strains of the species of the genus and 46 strains of Achromobacter species showed congruence between the cluster analyses derived from the individual genes. The MLSA gene sequences exhibited different levels of resolution in delineating the validly published Achromobacter species and elucidated strains that represent new genotypes and probable new species of the genus. Our results also suggested that the recently described A. spritinus is a later heterotypic synonym of A. marplatensis. Strains were analyzed, using whole-cell Matrix-Assisted Laser Desorption/Ionization Time-Of-Flight mass spectrometry (MALDI-TOF MS), as an alternative phenotypic profile-based method with the potential to support the identifications determined by the genotypic DNA sequencebased MLSA. The MALDI-TOF MS data showed good accordance in strain groupings and identifications by the MLSA data. Copyright, Margarita Gomila is the recipient of a postdoctoral contract from the University of the Balearic Islands funded by the Spanish Ministry of Education, Culture and Sports through the International Excellence Campus Program. Margarita Gomila was supported for exchange to the CCUG through fellowships from the Spanish Ministry of Education and Science, by means of the José Castillejo Program (2008) and from a FEMS Research Fellowship 2009-1. This work was supported also by funding from Västra Götaland Region (Sweden) projects ALFGBG-210591, VGFOUREG-157801 and VGFOUREG-232981, and from Spanish MINECO, through projects CGL2011-24318 and Consolider CSD2009-00006

Regeneration is the ability that allows organisms to replace missing organs or lost tissue after injuries. This ability requires the coordinated activity of different cellular processes, including programmed cell death. Apoptosis plays a key role as a source of signals necessary for regeneration in different organisms. The imaginal discs of Drosophila melanogaster provide a particularly well-characterised model system for studying the cellular and molecular mechanisms underlying regeneration. Although it has been shown that signals produced by apoptotic cells are needed for homeostasis and regeneration of some tissues of this organism, such as the adult midgut, the contribution of apoptosis to disc regeneration remains unclear. Using a new method for studying disc regeneration in physiological conditions, we have defined the pattern of cell death in regenerating discs. Our data indicate that during disc regeneration, cell death increases first at the wound edge, but as regeneration progresses dead cells can be observed in regions far away from the site of damage. This result indicates that apoptotic signals initiated in the wound spread throughout the disc. We also present results which suggest that the partial inhibition of apoptosis does not have a major effect on disc regeneration. Finally, our results suggest that during disc regeneration distinct apoptotic signals might be acting simultaneously., MEC (BFU2014-54153-P). SDG was supported by an FPI fellowship from the MICINN

This is an open-access article distributed under the terms of the Creative Commons Attribution License., Climate is one of the main drivers of species distribution. However, as different environmental factors tend to co-vary, the effect of climate cannot be taken at face value, as it may be either inflated or obscured by other correlated factors. We used the favourability models of four species (Alytes dickhilleni, Vipera latasti, Aquila fasciata and Capra pyrenaica) inhabiting Spanish mountains as case studies to evaluate the relative contribution of climate in their forecasted favourability by using variation partitioning and weighting the effect of climate in relation to non-climatic factors. By calculating the pure effect of the climatic factor, the pure effects of non-climatic factors, the shared climatic effect and the proportion of the pure effect of the climatic factor in relation to its apparent effect (ρ), we assessed the apparent effect and the pure independent effect of climate. We then projected both types of effects when modelling the future favourability for each species and combination of AOGCM-SRES (two Atmosphere-Ocean General Circulation Models: CGCM2 and ECHAM4, and two Special Reports on Emission Scenarios (SRES): A2 and B2). The results show that the apparent effect of climate can be either inflated (overrated) or obscured (underrated) by other correlated factors. These differences were species-specific; the sum of favourable areas forecasted according to the pure climatic effect differed from that forecasted according to the apparent climatic effect by about 61% on average for one of the species analyzed, and by about 20% on average for each of the other species. The pure effect of future climate on species distributions can only be estimated by combining climate with other factors. Transferring the pure climatic effect and the apparent climatic effect to the future delimits the maximum and minimum favourable areas forecasted for each species in each climate change scenario., The research was funded by the Ministerio de Ciencia e Innovación of Spain and FEDER (project CGL2009-11316/BOS). D. Romero is a PhD student at the University of Malaga with a grant of the Ministerio de Educación y Ciencia (AP 2007-03633).

This is an open-access article distributed under the terms of the Creative Commons Attribution License., The protein tyrosine phosphatase LYP, a key regulator of TCR signaling, presents a single nucleotide polymorphism, C1858T, associated with several autoimmune diseases such as type I diabetes, rheumatoid arthritis, and lupus. This polymorphism changes an R by a W in the P1 Pro rich motif of LYP, which binds to CSK SH3 domain, another negative regulator of TCR signaling. Based on the analysis of the mouse homologue, Pep, it was proposed that LYP and CSK bind constitutively to inhibit LCK and subsequently TCR signaling. The detailed study of LYP/CSK interaction, here presented, showed that LYP/CSK interaction was inducible upon TCR stimulation, and involved LYP P1 and P2 motifs, and CSK SH3 and SH2 domains. Abrogating LYP/CSK interaction did not preclude the regulation of TCR signaling by these proteins., This work was supported by a grant (SAF2009-09724) from Ministerio de Ciencia e Innovación (MICINN,http://www.idi.mineco.gob.es/portal/site​/MICINN), by Fundación Mutua Madrileña (http://www.fundacionmutua.es), and by Red Cardiovascular (RECAVA) from Instituto de Salud Carlos III (http://www.recava.com). Y. Bayón has been under contract within the Ramón y Cajal Program of the Ministerio de Educación y Ciencia of Spain, co-funded by the European Social Fund through FEDER-FSE (http://www.educacion.gob.es).

This is an open-access article distributed under the terms of the Creative Commons Attribution License.-- et al., [Context]: Expression and activity of the main lipogenic enzymes is paradoxically decreased in obesity, but the mechanisms behind these findings are poorly known. Breast Cancer 1 (BrCa1) interacts with acetyl-CoA carboxylase (ACC) reducing the rate of fatty acid biosynthesis. In this study, we aimed to evaluate BrCa1 in human adipose tissue according to obesity and insulin resistance, and in vitro cultured adipocytes. [Research Design and Methods]: BrCa1 gene expression, total and phosphorylated (P-) BrCa1, and ACC were analyzed in adipose tissue samples obtained from a total sample of 133 subjects. BrCa1 expression was also evaluated during in vitro differentiation of human adipocytes and 3T3-L1 cells. [Results]: BrCa1 gene expression was significantly up-regulated in both omental (OM; 1.36-fold, p = 0.002) and subcutaneous (SC; 1.49-fold, p = 0.001) adipose tissue from obese subjects. In parallel with increased BrCa1 mRNA, P-ACC was also up-regulated in SC (p = 0.007) as well as in OM (p = 0.010) fat from obese subjects. Consistent with its role limiting fatty acid biosynthesis, both BrCa1 mRNA (3.5-fold, p, This work was supported by research grants from the Ministerio de Educación y Ciencia SAF2008-02073 and SAF2009-10461), the Fundación Mutua Madrileña, and the Instituto de Salud Carlos III (ISCIIIRETIC RD06, CIBERObN).

Porous ceramic scaffolds are widely studied in the tissue engineering field due to their potential in medical applications as bone substitutes or as bone-filling materials. Solid free form (SFF) fabrication methods allow fabrication of ceramic scaffolds with fully controlled pore architecture, which opens new perspectives in bone tissue regeneration materials. However, little experimentation has been performed about real biological properties and possible applications of SFF designed 3D ceramic scaffolds. Thus, here the biological properties of a specific SFF scaffold are evaluated first, both in vitro and in vivo, and later scaffolds are also implanted in pig maxillary defect, which is a model for a possible application in maxillofacial surgery. In vitro results show good biocompatibility of the scaffolds, promoting cell ingrowth. In vivo results indicate that material on its own conducts surrounding tissue and allow cell ingrowth, thanks to the designed pore size. Additional osteoinductive properties were obtained with BMP-2, which was loaded on scaffolds, and optimal bone formation was observed in pig implantation model. Collectively, data show that SFF scaffolds have real application possibilities for bone tissue engineering purposes, with the main advantage of being fully customizable 3D structures. This work was supported by Ministerio de Ciencia e Innovación (PET2008-0168, CSD2009-00088), and Ministerio de Educación y Ciencia y Fondo Social Europeo (PTQ05-02-02498 and Fundación PCM, MAT 2006-08720). These funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. Escherichia-coli-produced recombinant human BMP-2 (rhBMP-2) was generously supplied by Noricum S.L. (Spain). We thank Alba Cuenca-Moya (Noricum S.L.) and Virginia Gutierrez (Pharmakine) for their technical support. Sí

Received: July 6, 2012; Accepted: November 13, 2012; Published: December 13, 2012, Habitat selection is a crucial decision for any organism. Selecting a high quality site will positively impact survival and reproductive output. Predation risk is an important component of habitat quality that is known to impact reproductive success and individual condition. However, separating the breeding consequences of decision-making of wild animals from individual quality is difficult. Individuals face reproductive decisions that often vary with quality such that low quality individuals invest less. This reduced reproductive performance could appear a cost of increased risk but may simply reflect lower quality. Thus, teasing apart the effects of individual quality and the effect of predation risk is vital to understand the physiological and reproductive costs of predation risk alone on breeding animals. In this study we alter the actual territory location decisions of pied flycatchers by moving active nests relative to breeding sparrowhawks, the main predators of adult flycatchers. We experimentally measure the non-lethal effects of predation on adults and offspring while controlling for effects of parental quality, individual territory choice and initiation of breeding. We found that chicks from high predation risk nests (200 m from hawk). However, in contrast to correlative results, females in manipulated high risk nests did not suffer decreased body condition or increased stress response (HSP60 and HSP70). Our results suggest that territory location decisions relative to breeding avian predators cause spatial gradients in individual quality. Small adjustments in territory location decisions have crucial consequences and our results confirm non-lethal costs of predation risk that were expressed in terms of smaller offspring produced. However, females did not show costs in physiological condition which suggests that part of the costs incurred by adults exposed to predation risk are quality determined., This work was supported by: Oskar Öflund's foundation, Ella and Georg Ehrnrooth foundation and the Academy of Finland (project number 138049) to RT; Academy of Finland (project numbers: 122665 and 125720) to JF; Programme Juan de la Cierva and Grant BOS 2003-05724 from Ministerio de Educación y Ciencia to GT.

Martin Sikora et al., A large proportion of the death toll associated with malaria is a consequence of malaria infection during pregnancy, causing up to 200,000 infant deaths annually. We previously published the first extensive genetic association study of placental malaria infection, and here we extend this analysis considerably, investigating genetic variation in over 9,000 SNPs in more than 1,000 genes involved in immunity and inflammation for their involvement in susceptibility to placental malaria infection. We applied a new approach incorporating results from both single gene analysis as well as gene-gene interactions on a protein-protein interaction network. We found suggestive associations of variants in the gene KLRK1 in the single gene analysis, as well as evidence for associations of multiple members of the IL-7/IL-7R signalling cascade in the combined analysis. To our knowledge, this is the first large-scale genetic study on placental malaria infection to date, opening the door for follow-up studies trying to elucidate the genetic basis of this neglected form of malaria., This work was supported by grant SAF-2007-63171 awarded by Ministerio de Educación y Ciencia (Spain) to JB and the CIBERESP (CIBER of Epidemiology and Public Health, Ministry of Health). Funds were also obtained from Dirreció General de Recerca of Generalitat de Catalunya (Grup de Recerca Consolidat 2005SGR/00608) and from Banco de Bilbao, Vizcaya, Argentaria Foundation (grant number BBVA 02-0). The CISM receives core support from the Spanish Agency for International Cooperation and Development (AECID). All the genotyping was provided by the Spanish “Centro Nacional de Genotipado” (CEGEN; www.cegen.org); support for computations was provided by the National Institute for Bioinformatics (www.inab.org); both are platforms of Genoma España. MGN was supported by a Vici grant of the Netherlands Organization for Scientific Research. AM was supported by the Spanish Ministry of Health (Program for the Promotion of Biomedical Research and Health Sciences, Instituto de Salud Carlos III, CP-04/00220). MS was supported by a PhD fellowship from the Programa de becas FPU del Ministerio de Educación y Ciencia, Spain (AP2005-3982).

13 páginas, 6 figuras., This is an open-access article distributed under the terms of the Creative Commons Attribution License., The SWR1 complex replaces the canonical histone H2A with the variant H2A.Z (Htz1 in yeast) at specific chromatin regions. This dynamic alteration in nucleosome structure provides a molecular mechanism to regulate transcription, gene silencing, chromosome segregation and DNA repair. Here we show that genetic instability, sensitivity to drugs impairing different cellular processes and genome-wide transcriptional misregulation in htz1Δ can be partially or totally suppressed if SWR1 is not formed (swr1Δ), if it forms but cannot bind to chromatin (swc2Δ) or if it binds to chromatin but lacks histone replacement activity (swc5Δ and the ATPase-dead swr1-K727G). These results suggest that in htz1Δ the nucleosome remodelling activity of SWR1 affects chromatin integrity because of an attempt to replace H2A with Htz1 in the absence of the latter. This would impair transcription and, either directly or indirectly, other cellular processes. Specifically, we show that in htz1Δ, the SWR1 complex causes an accumulation of recombinogenic DNA damage by a mechanism dependent on phosphorylation of H2A at Ser129, a modification that occurs in response to DNA damage, suggesting that the SWR1 complex impairs the repair of spontaneous DNA damage in htz1Δ. In addition, SWR1 causes DSBs sensitivity in htz1Δ; consistently, in the absence of Htz1 the SWR1 complex bound near an endonuclease HO-induced DSB at the mating-type (MAT) locus impairs DSB-induced checkpoint activation. Our 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., The research was funded by the Spanish Ministry of Education and Science (BFU2006-08336 grant) and the Junta de Andalucia (P07-CVI-032000). M.C-R. was a recipient of a pre-doctoral training grant from the Spanish Research Council (CSIC). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

This is an open-access article distributed under the terms of the Creative Commons Attribution License., [Background]: Three functional c-ras genes, known as c-H-ras, c-K-ras, and c-N-ras, have been largely studied in mammalian cells with important insights into normal and tumorigenic cellular signal transduction events. Two K-Ras mRNAs are obtained from the same pre-mRNA by alternative splicing. H-Ras pre-mRNA can also be alternatively spliced in the IDX and 4A terminal exons, yielding the p19 and p21 proteins, respectively. However, despite the Ras gene family’s established role in tumorigenic cellular signal transduction events, little is known about p19 function. Previous results showed that p19 did not interact with two known p21 effectors, Raf1 and Rin1, but was shown to interact with RACK1, a scaffolding protein that promotes multi-protein complexes in different signaling pathways (Cancer Res 2003, 63 p5178). This observation suggests that p19 and p21 play differential and complementary roles in the cell., [Principal Findings]: We found that p19 regulates telomerase activity through its interaction with p73a/b proteins. We also found that p19 overexpression induces G1/S phase delay; an observation that correlates with hypophosphorylation of both Akt and p70SK6. Similarly, we also observed that FOXO1 is upregulated when p19 is overexpressed. The three observations of (1) hypophosphorylation of Akt, (2) G1/S phase delay and (3) upregulation of FOXO1 lead us to conclude that p19 induces G1/S phase delay, thereby maintaining cells in a reversible quiescence state and preventing entry into apoptosis. We then assessed the effect of p19 RNAi on HeLa cell growth and found that p19 RNAi increases cell growth, thereby having the opposite effect of arrest of the G1/S phase or producing a cellular quiescence state., [Significance]: Interestingly, p19 induces FOXO1 that in combination with the G1/S phase delay and hypophosphorylation of both Akt and p70SK6 leads to maintenance of a reversible cellular quiescence state, thereby preventing entry into apoptosis., This work was supported by Fundacion de Investigacion Medica Mutua Madrileña Automovilista (Fundacion MMA), the Plan Nacional (MEC) BFU2005-00701 and the Fundacion Eugenio Rodriguez Pascual. M.C. was a recipient of a Fmed MMA fellowship.

PLoS ONE 4(10): e7290., Background: DNA polymerase lambda (Poll) is a DNA repair polymerase, which likely plays a role in base excision repair (BER) and in non-homologous end joining (NHEJ) of DNA double-strand breaks (DSB). Principal Findings: Here, we described a novel natural allelic variant of human Poll (hPoll) characterized by a single nucleotide polymorphism (SNP), C/T variation in the first base of codon 438, resulting in the amino acid change Arg to Trp. In vitro enzyme activity assays of the purified W438 Poll variant revealed that it retained both DNA polymerization and deoxyribose phosphate (dRP) lyase activities, but had reduced base substitution fidelity. Ectopic expression of the W438 hPoll variant in mammalian cells increases mutation frequency, affects the DSB repair NHEJ pathway, and generates chromosome aberrations. All these phenotypes are dependent upon the catalytic activity of the W438 hPoll. Conclusions: The expression of a cancer-related natural variant of one specialized DNA polymerase can be associated to generic instability at the cromosomal level, probably due a defective NHEJ. These results establish that chromosomal aberrations can result from mutations in specialized DNA repair polymerases., This work was supported by Ministerio de Ciencia y Tecnologia Grants BFU2006-14390/BMC, CONSOLIDER CSD2007-00015 and Comunidad Autonoma de Madrid Grants P2006/BIO-0306 to L.B., by INCa ‘‘Checkpol’’, ARC, and ‘‘Ligue contre le Cancer (Region Midi-Pyrenees)’’ to J-S.H., by the Division of Intramural Research, NIEHS, NIH, DHHS to T.A.K., by SAF2002-02265 to A.V., and by an institutional grant to Centro de Biologia Molecular ‘‘Severo Ochoa’’ from Fundacion Ramon Areces. G.T. was recipient of a fellowship from the Ministerio de Educacion y Ciencia. A.V. is an Investigator of the Ramon y Cajal Program

This is an open-access article distributed under the terms of the Creative Commons Attribution License., [Background]: H-Ras pre-mRNA undergoes an alternative splicing process to render two H-Ras, due to either the exclusion or inclusion of the alternative intron D exon (IDX), known to reduce IDX inclusion. [Principal Findings]: Here we show that p68 unwinds the stem-loop IDX-rasISS1 structure to IDX-rasISS1. We also found that p68 alters the dynamic localization of SC35, a splicing The knockdown of hnRNP A1, FUS/TLS and hnRNP H resulted in upregulation of the SC35-binding protein, SFRS2IP. Finally, FUS/TLS was observed to upregulate p19 expression and in vivo RNAi-mediated depletion of hnRNP H decreased p19 H-Ras abundance. [Significance]: Taken together, p68 is shown to be an essential player in the regulation transduction signal pathway tied to cell proliferation and many cancer processes., This work was supported by Fundación de Investigación Médica Mútua Madrileña Automovilista (Fundación MMA) and by the Plan Nacional (MEC) BFU2005-00701. M.C., S.G and M.K. were recipients of a Fmed MMA, BEFI (Carlos III) and FPU (MEC) fellowships, respectively.

This work was funded by the Ministerio de Ciencia e Innovacion (MICINN) grants (SAF2008-00211; PIE- 200820I166), and a grant from the Spanish Comunidad de Madrid CCG08-CSIC/SAL-3464. G-protein-coupled receptors (GPCRs) are known to activate both G protein- and β -arrestin-dependent signalling cascades. The initiation of mitogen-activated protein kinase (MAPK) pathways is a key downstream event in the control of cellular functions including proliferation, differentiation, migration and apoptosis. Both G proteins and β-arrestins have been reported to mediate context-specific activation of ERK1/2, p38 and JNK MAPKs. Recently, the activation of ERK5 MAPK by Gq-coupled receptors has been described to involve a direct interaction between G αqand two novel effectors, PKCζ and MEK5. However, the possible contribution of β-arrestin towards this pathway has not yet been addressed. In the present work we sought to investigate the role of receptor internalization processes and β-arrestin recruitment in the activation of ERK5 by Gq-coupled GPCRs. Our results show that ERK5 activation is independent of M1 or M3 muscarinic receptor internalization. Furthermore, we demonstrate that phosphorylation-deficient muscarinic M1 and M3 receptors are still able to fully activate the ERK5 pathway, despite their reported inability to recruit β-arrestins. Indeed, the overexpression of Gαq, but not that of β-arrestin1 or β-arrestin2, was found to potently enhance ERK5 activation by GPCRs, whereas silencing of β-arrestin2 expression did not affect the activation of this pathway. Finally, we show that a β-arrestin-biased mutant form of angiotensin II (SII; Sar1-Ile4-Ile8AngII) failed to promote ERK5 phosphorylation in primary cardiac fibroblasts, as compared to the natural ligand. Overall, this study shows that the activation of ERK5 MAPK by model Gq-coupled GPCRs does not depend on receptor internalization, β-arrestin recruitment or receptor phosphorylation but rather is dependent on Gαq-signalling., The study was funded by grants from Ministerio de Educación y Ciencia (SAF2011-23800), Fundación Ramón Areces, The Cardiovascular Diseases Network of Ministerio Sanidad y Consumo-Instituto Carlos III (RD12/0042/0012), Comunidad de Madrid (S-2011/BMD-2332) and Instituto de Salud Carlos III (PI11/00126). Collaboration with Dr. Andrew Tobin was possible thanks to a Wood-Whelan Research Felowship (IUMBM) awarded to GSF. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

Received: April 5, 2013; Accepted: August 23, 2013; Published: October 4, 2013, In this paper we describe a new type of subterranean habitat associated with dry watercourses in the Eastern Iberian Peninsula, the “Alluvial Mesovoid Shallow Substratum” (alluvial MSS). Historical observations and data from field sampling specially designed to study MSS fauna in the streambeds of temporary watercourses support the description of this new habitat. To conduct the sampling, 16 subterranean sampling devices were placed in a region of Eastern Spain. The traps were operated for 12 months and temperature and relative humidity data were recorded to characterise the habitat. A large number of species was captured, many of which belonged to the arthropod group, with marked hygrophilous, geophilic, lucifugous and mesothermal habits. In addition, there was also a substantial number of species showing markedly ripicolous traits. The results confirm that the network of spaces which forms in alluvial deposits of temporary watercourses merits the category of habitat, and here we propose the name of “alluvial MSS”. The “alluvial MSS” may be covered or not by a layer of soil, is extremely damp, provides a buffer against above ground temperatures and is aphotic. In addition, compared to other types of MSS, it is a very unstable habitat. It is possible that the “alluvial MSS” may be found in other areas of the world with strongly seasonal climatic regimes, and could play an important role as a biogeographic corridor and as a refuge from climatic changes., The Spanish Ministry of Science and Innovation for funded this research project (CGL2010-19924) and the Ministry of Education and Science programme "Juan de la Cierva". This research Project (CGL2010-19924) was funded by the Spanish Ministry of Science and Innovation., The Ministry of Education and Science programme "Juan de la Cierva" funded the research activity of one of the authors (A. J-V.).

In winter, foraging activity is intended to optimize food search while minimizing both thermoregulation costs and predation risk. Here we quantify the relative importance of thermoregulation and predation in foraging patch selection of woodland birds wintering in a Mediterranean montane forest. Specifically, we account for thermoregulation benefits related to temperature, and predation risk associated with both illumination of the feeding patch and distance to the nearest refuge provided by vegetation. We measured the amount of time that 38 marked individual birds belonging to five small passerine species spent foraging at artificial feeders. Feeders were located in forest patches that vary in distance to protective cover and exposure to sun radiation; temperature and illumination were registered locally by data loggers. Our results support the influence of both thermoregulation benefits and predation costs on feeding patch choice. The influence of distance to refuge (negative relationship) was nearly three times higher than that of temperature (positive relationship) in determining total foraging time spent at a patch. Light intensity had a negligible and no significant effect. This pattern was generalizable among species and individuals within species, and highlights the preponderance of latent predation risk over thermoregulation benefits on foraging decisions of birds wintering in temperate Mediterranean forests. © 2013 Villén-Pérez et al., This paper was funded by project CGL2008-02211/BOS of the Spanish Ministry of Educación y Ciencia.

A definitive consequence of the aging process is the progressive deterioration of higher cognitive functions. Defects in DNA repair mechanisms mostly result in accelerated aging and reduced brain function. DNA polymerase ο is a novel accessory partner for the non-homologous end-joining DNA repair pathway for double-strand breaks, and its deficiency causes reduced DNA repair. Using associative learning and long-term potentiation experiments, we demonstrate that Polο-/- mice, however, maintain the ability to learn at ages when wild-type mice do not. Expression and biochemical analyses suggest that brain aging is delayed in Polο-/- mice, being associated with a reduced error-prone DNA oxidative repair activity and a more efficient mitochondrial function. This is the first example in which the genetic ablation of a DNA-repair function results in a substantially better maintenance of learning abilities, together with fewer signs of brain aging, in old mice. © 2013 Lucas et al., Ministerio de Ciencia e innovación (BFU2008-03390/BMC/MICINN), (BFU2008-00899/MICINN),BFU2007-60263/MICINN; PAC08-0261-1581/JCCM, SAF 2008-02099/MICINN, PLE2009-0147; Spanish Ministry of Education ; Fundación Ramón Areces

This is an open-access article distributed under the terms of the Creative Commons Attribution License., Cell polarization is key for the function of most eukaryotic cells, and regulates cell shape, migration and tissue architecture. Fission yeast, Schizosaccharomyces pombe cells are cylindrical and polarize cell growth to one or both cell tips dependent on the cell cycle stage. Whereas microtubule cytoskeleton contributes to the positioning of the growth sites by delivering polarity factors to the cell ends, the Cdc42 GTPase polarizes secretion via actin-dependent delivery and tethering of secretory vesicles to plasma membrane. How growth is restricted to cell tips and how re-initiation of tip growth is regulated in the cell cycle remains poorly understood. In this work we investigated the function of protein phosphatase type 2A (PP2A) in S. pombe morphogenesis by deleting the evolutionary conserved PTPA-type regulatory subunit that we named pta2. pta2-deleted cells showed morphological defects and altered growth pattern. Consistent with this, actin patches and active Cdc42 were mislocalized in the pta2 deletion. These defects were additive to the lack of Cdc42-GAP Rga4. pta2Δ cells show upregulated Cdc42 activity and pta2 interacts genetically with polarisome components Tea1, Tea4 and For3 leading to complete loss of cell polarity and rounded morphology. Thus, regulation of polarity by PP2A requires the polarisome and involves Pta2-dependent control of Cdc42 activity., This work was supported by grants to RRD from the Spanish Ministerio de Ciencia e Inovación BFU2010-21310 and P09-CTS-4697 (PROYECTO DE EXCELENCIA) from La Junta de Andalucia. MB was supported by Spanish Ministerio de Educación (FPI Fellowship, BES-2008-004018).