LIGHT-COLOR-INDUCED CHANGES IN FATTY ACID BIOSYNTHESIS IN Chlorella sp. STRAIN KS-MA2 IN EARLY STATIONARY GROWTH PHASE

Optimization of light supply remains a critical issue in microalgae biotechnology. The impacts of light color on fatty acid production and biosynthesis in microalgae are poorly understood. The aim of this study was to determine the effect of light color on growth and fatty acid content in Chlorella strain KS-MA2. Cells were cultured on F/2 medium and incubated under blue, green, red or white light. The cells’ growth, fatty acid composition and the expression levels of the ketoacyl synthase 1 (KAS-1), omega-6 desaturase (ω-6 FAD) and omega-3 desaturase (ω-3 FAD) genes were measured at the early stationary growth phase. Results of this study indicated that light color affected cell density and fatty acid profile produced by Chlorella sp. strain KS-MA2. Cells cultured under blue, red and white light had higher cell density than those cultured under green light. Palmitic acid (38.62 ± 3.29% of biomass dry weight) and linolenic acid (7.96 ± 0.88% of biomass dry weight) were highly accumulated under white light. Stearic acid was dominant under blue light (11.11 ± 0.14% of biomass dry weight), whereas oleic acid was dominant under red light (30.50 ± 0.14% of biomass dry weight). Linoleic acid was highly produced under green and blue light (28.63 ± 1.36% and 26.00 ± 0.81 % of biomass dry weight, respectively). KAS-1 and ω-6 FAD were highly expressed under blue light, whereas ω-3 FAD was highly expressed under green light. The production of particular fatty acids of interest from Chlorella could be achieved by shifting color of light used during the incubation of the cell cultures. Blue-light is the most suitable light color for producing biomass and stearic acid by Chlorellastrain KS-MA2.Â

Longitudinal study to assess changes in arterial stiffness and cardiac output parameters among low-risk pregnant women.

AIM: A single-centre, prospective longitudinal study to assess changes in maternal arterial stiffness and cardiac output parameters among low-risk healthy pregnant women. METHODOLOGY: Thirty low-risk, healthy, pregnant women attending their routine antenatal dating ultrasound scan were recruited. Non-invasive assessment of arterial stiffness and cardiac output was undertaken at five gestational windows from 11 to 40 weeks of pregnancy. Data were analysed using a linear mixed model incorporating time and other relevant predictors as fixed effects, and patient as a random effect. RESULTS: Gestational age had a significant effect on all arterial stiffness parameters, including brachial augmentation index (AIx) (p = .001), aortic AIx (p = .002) and aortic pulse wave velocity (p = .002). The aortic AIx (%) reduced during pregnancy: the lowest mean (standard error, SE) was 4.07 (1.01) at 28 weeks before it increased to 7.04 (SE 1.64) at 40 weeks. Similarly, non-invasive assessments of cardiac output (p < .001), stroke volume (p = .014), heart rate (p < .001) and total peripheral resistance (p < .001) demonstrated significant changes with gestational age. Mean cardiac output (l/m) increased during pregnancy reaching a peak at 28 weeks gestation 6.66 (SE 0.28), but dropped thereafter to reach 5.71 (SE 0.25) around term. CONCLUSION: The current study provides pregnancy normograms for gestational changes in arterial stiffness and cardiac output parameters among low-risk, healthy pregnant women. Further work will be required to assess the risk of placental mediated diseases and pregnancy outcome among pregnant women with parameters outside the normal range

Ultrafine anaphase bridges, broken DNA and illegitimate recombination induced by a replication fork barrier

Most DNA double-strand breaks (DSBs) in S- and G2-phase cells are repaired accurately by Rad51-dependent sister chromatid recombination. However, a minority give rise to gross chromosome rearrangements (GCRs), which can result in disease/death. What determines whether a DSB is repaired accurately or inaccurately is currently unclear. We provide evidence that suggests that perturbing replication by a non-programmed protein–DNA replication fork barrier results in the persistence of replication intermediates (most likely regions of unreplicated DNA) into mitosis, which results in anaphase bridge formation and ultimately to DNA breakage. However, unlike previously characterised replication-associated DSBs, these breaks are repaired mainly by Rad51-independent processes such as single-strand annealing, and are therefore prone to generate GCRs. These data highlight how a replication-associated DSB can be predisposed to give rise to genome rearrangements in eukaryotes

In vitro propagation of Vitis vinifera L. cv. 'Monastrell'

[EN] Background: A protocol for the micropropagation of the grape (Vitis vinifera L.) cultivar 'Monastrell' was developed. Initial plant material was obtained from the sanitary selection of grapevine plants performed by real-time RT-PCR to confirm the absence of Grapevine fanleaf virus, Arabis mosaic virus, Grapevine leafroll-associated virus 1, Grapevine leafroll-associated virus 3, and Grapevine fleck virus. Results: The effects of the salt composition (comparing Lloyd and McCown woody plant medium and Murashige and Skoog medium 1/2 macronutrients) and the growth regulator benzylaminopurine (BAP), at 0 and 8.9 mu M, on plant propagation were evaluated using nodes as explants. The most efficient procedure consisted of bud induction in the medium with Lloyd and McCown woody plant salts and 8.9 mu M BAP for 30 d along with elongation in cytokinin-free medium for 60 d, which gave 22 nodes/explant (174 plants/initial plant). A second cycle of propagation in a medium without BAP for another 60 d could give approximately 10,000 nodes, which can be obtained after an additional 2 months of culture. All plants acclimatized after the second cycle of multiplication were successfully transferred to soil. Conclusion: We developed an optimal protocol for V. vinifera cv. 'Monastrell' micropropagation, the first described for this cultivar. (C) 2017 Pontificia Universidad Catolica de Valparaiso. Production and hosting by Elsevier B. V. All rights reserved.The study was supported by the projects RTA2011-00067-C04, RTA2014-00061-C03, and PRP-CGL2015-70843-R, all co-funded with FEDER Funds. Tania San Pedro has a grant (01/14-FSE-22) supported by the Instituto Valenciano de Investigaciones Agrarias.San Pedro-Galan, T.; Peiró Barber, RM.; Villanova, J.; Olmos Castelló, A.; Gisbert Domenech, MC. (2017). In vitro propagation of Vitis vinifera L. cv. 'Monastrell'. Electronic Journal of Biotechnology. 27:80-83. https://doi.org/10.1016/j.ejbt.2017.03.006S80832

Human Fbh1 helicase contributes to genome maintenance via pro- and anti-recombinase activities

Human Fbh1 helicase contributes to genome maintenance via pro- and anti-recombinase activities

Mug20, a novel protein associated with linear elements in fission yeast meiosis

In the fission yeast, Schizosaccharomyces pombe, homologous chromosomes efficiently pair and recombine during meiotic prophase without forming a canonical synaptonemal complex (SC). Instead, it features simpler filamentous structures, the so-called linear elements (LinEs), which bear some resemblance to the axial/lateral element subunits of the SC. LinEs are required for wild-type recombination frequency. Here, we recognized Mug20, the product of a meiotically upregulated gene, as a LinE-associated protein. GFP-tagged Mug20 and anti-Mug20 antibody co-localized completely with Rec10, one of the major constituents of LinEs. In the absence of Mug20, LinEs failed to elongate beyond their initial state of nuclear dots. Foci of recombination protein Rad51 and genetic recombination were reduced. Since meiotic DNA double-strand breaks (DSBs), which initiate recombination, are induced at sites of preformed LinEs, we suggest that reduced recombination is a consequence of incomplete LinE extension. Therefore, we propose that Mug20 is required to extend LinEs from their sites of origin and thereby to increase DSB proficient regions on chromosomes

Multiagent systems

Our future is that of a mixed society of people and AI artifacts. A multitude of devices in our homes will need not only to make intelligent decisions, but they will also need to coordinate with each other to serve us well. Cars will have to coordinate to allow safe road crossings, avoiding accidents. Also, the industry is already beginning to integrate teams of humans and robots collaborating to solve complex problems...Peer reviewe

Cooperation of RAD51 and RAD54 in regression of a model replication fork

DNA lesions cause stalling of DNA replication forks, which can be lethal for the cell. Homologous recombination (HR) plays an important role in DNA lesion bypass. It is thought that Rad51, a key protein of HR, contributes to the DNA lesion bypass through its DNA strand invasion activity. Here, using model stalled replication forks we found that RAD51 and RAD54 by acting together can promote DNA lesion bypass in vitro through the ‘template-strand switch’ mechanism. This mechanism involves replication fork regression into a Holliday junction (‘chicken foot structure’), DNA synthesis using the nascent lagging DNA strand as a template and fork restoration. Our results demonstrate that RAD54 can catalyze both regression and restoration of model replication forks through its branch migration activity, but shows strong bias toward fork restoration. We find that RAD51 modulates this reaction; by inhibiting fork restoration and stimulating fork regression it promotes accumulation of the chicken foot structure, which we show is essential for DNA lesion bypass by DNA polymerase in vitro. These results indicate that RAD51 in cooperation with RAD54 may have a new role in DNA lesion bypass that is distinct from DNA strand invasion

Localization of recombination proteins and Srs2 reveals anti-recombinase function in vivo

Homologous recombination (HR), although an important DNA repair mechanism, is dangerous to the cell if improperly regulated. The Srs2 “anti-recombinase” restricts HR by disassembling the Rad51 nucleoprotein filament, an intermediate preceding the exchange of homologous DNA strands. Here, we cytologically characterize Srs2 function in vivo and describe a novel mechanism for regulating the initiation of HR. We find that Srs2 is recruited separately to replication and repair centers and identify the genetic requirements for recruitment. In the absence of Srs2 activity, Rad51 foci accumulate, and surprisingly, can form in the absence of Rad52 mediation. However, these Rad51 foci do not represent repair-proficient filaments, as determined by recombination assays. Antagonistic roles for Rad52 and Srs2 in Rad51 filament formation are also observed in vitro. Furthermore, we provide evidence that Srs2 removes Rad51 indiscriminately from DNA, while the Rad52 protein coordinates appropriate filament reformation. This constant breakdown and rebuilding of filaments may act as a stringent quality control mechanism during HR

Multiple Analytical Approaches Reveal Distinct Gene-Environment Interactions in Smokers and Non Smokers in Lung Cancer

Complex disease such as cancer results from interactions of multiple genetic and environmental factors. Studying these factors singularly cannot explain the underlying pathogenetic mechanism of the disease. Multi-analytical approach, including logistic regression (LR), classification and regression tree (CART) and multifactor dimensionality reduction (MDR), was applied in 188 lung cancer cases and 290 controls to explore high order interactions among xenobiotic metabolizing genes and environmental risk factors. Smoking was identified as the predominant risk factor by all three analytical approaches. Individually, CYP1A1*2A polymorphism was significantly associated with increased lung cancer risk (OR = 1.69;95%CI = 1.11–2.59,p = 0.01), whereas EPHX1 Tyr113His and SULT1A1 Arg213His conferred reduced risk (OR = 0.40;95%CI = 0.25–0.65,p<0.001 and OR = 0.51;95%CI = 0.33–0.78,p = 0.002 respectively). In smokers, EPHX1 Tyr113His and SULT1A1 Arg213His polymorphisms reduced the risk of lung cancer, whereas CYP1A1*2A, CYP1A1*2C and GSTP1 Ile105Val imparted increased risk in non-smokers only. While exploring non-linear interactions through CART analysis, smokers carrying the combination of EPHX1 113TC (Tyr/His), SULT1A1 213GG (Arg/Arg) or AA (His/His) and GSTM1 null genotypes showed the highest risk for lung cancer (OR = 3.73;95%CI = 1.33–10.55,p = 0.006), whereas combined effect of CYP1A1*2A 6235CC or TC, SULT1A1 213GG (Arg/Arg) and betel quid chewing showed maximum risk in non-smokers (OR = 2.93;95%CI = 1.15–7.51,p = 0.01). MDR analysis identified two distinct predictor models for the risk of lung cancer in smokers (tobacco chewing, EPHX1 Tyr113His, and SULT1A1 Arg213His) and non-smokers (CYP1A1*2A, GSTP1 Ile105Val and SULT1A1 Arg213His) with testing balance accuracy (TBA) of 0.6436 and 0.6677 respectively. Interaction entropy interpretations of MDR results showed non-additive interactions of tobacco chewing with SULT1A1 Arg213His and EPHX1 Tyr113His in smokers and SULT1A1 Arg213His with GSTP1 Ile105Val and CYP1A1*2C in nonsmokers. These results identified distinct gene-gene and gene environment interactions in smokers and non-smokers, which confirms the importance of multifactorial interaction in risk assessment of lung cancer