Journal articles: 'RSC complex, Rsc2'

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Bungard, David, Michelle Reed, and Edward Winter. "RSC1 and RSC2 Are Required for Expression of Mid-Late Sporulation-Specific Genes in Saccharomyces cerevisiae." Eukaryotic Cell 3, no. 4 (August 2004): 910–18. http://dx.doi.org/10.1128/ec.3.4.910-918.2004.

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ABSTRACT Rsc1 and Rsc2 are alternative bromodomain-containing subunits of the ATP-dependent RSC chromatin remodeling complex in Saccharomyces cerevisiae. Smk1 is a sporulation-specific mitogen-activated protein kinase homolog that is required for the postmeiotic events of spore formation. In this study we show that RSC1 and RSC2 are haploinsufficient for spore formation in a smk1 hypomorph. Moreover, diploids lacking Rsc1 or Rsc2 show a subset of smk1-like phenotypes. High-copy-number RSC1 plasmids do not suppress rsc2-Δ/rsc2-Δ sporulation defects, and high-copy-number RSC2 plasmids do not suppress rsc1-Δ/rsc1-Δ sporulation defects. Mid-late sporulation-specific genes, which are normally expressed while key steps in spore assembly occur and which include genes that are required for spore wall formation, are not expressed in cells lacking Rsc1 or Rsc2. We speculate that the combined action of Rsc1 and Rsc2 at mid-late promoters is specifically required for the proper expression of this uniquely timed set of genes. Our data suggest that Smk1 and Rsc1/2 define parallel pathways that converge to provide signaling information and the expression of gene products, respectively, that are required for spore morphogenesis.

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Wong, Michael C. V. L., Suzanna R. S. Scott-Drew, Matthew J. Hayes, Philip J. Howard, and James A. H. Murray. "RSC2, Encoding a Component of the RSC Nucleosome Remodeling Complex, Is Essential for 2μm Plasmid Maintenance in Saccharomyces cerevisiae." Molecular and Cellular Biology 22, no. 12 (June 15, 2002): 4218–29. http://dx.doi.org/10.1128/mcb.22.12.4218-4229.2002.

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ABSTRACT The stable maintenance of the 2μm circle plasmid depends on its ability to overcome intrinsic maternal inheritance bias, which in yeast normally results in the failure to transmit DNA molecules efficiently to daughter cells. In addition to the plasmid proteins Rep1 and Rep2 acting on the plasmid DNA locus STB, it is likely that other chromosomally encoded yeast proteins are required. We have isolated mutants of yeast unable to maintain 2μm and found that RSC2 is essential for 2μm to overcome maternal inheritance bias. Rsc2 is part of a multisubunit RSC chromatin remodeling complex, and we show that in the absence of Rsc2 the chromatin structure of the STB region is significantly altered and the Rep1 protein loses its normal localization to subnuclear foci. Rsc1, a closely related homolog of Rsc2 present in an alternative form of the RSC complex, is not required for 2μm maintenance and does not replace the requirement for Rsc2 when overexpressed. This represents the first specific role for Rsc2 that has been related to a change in chromatin structure, as well as the first direct evidence linking chromatin structure to 2μm segregation.

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Baetz, Kristin K., Nevan J. Krogan, Andrew Emili, Jack Greenblatt, and Philip Hieter. "The ctf13-30/CTF13 Genomic Haploinsufficiency Modifier Screen Identifies the Yeast Chromatin Remodeling Complex RSC, Which Is Required for the Establishment of Sister Chromatid Cohesion." Molecular and Cellular Biology 24, no. 3 (February 1, 2004): 1232–44. http://dx.doi.org/10.1128/mcb.24.3.1232-1244.2003.

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ABSTRACT The budding yeast centromere-kinetochore complex ensures high-fidelity chromosome segregation in mitosis and meiosis by mediating the attachment and movement of chromosomes along spindle microtubules. To identify new genes and pathways whose function impinges on chromosome transmission, we developed a genomic haploinsufficiency modifier screen and used ctf13-30, encoding a mutant core kinetochore protein, as the reference point. We demonstrate through a series of secondary screens that the genomic modifier screen is a successful method for identifying genes that encode nonessential proteins required for the fidelity of chromosome segregation. One gene isolated in our screen was RSC2, a nonessential subunit of the RSC chromatin remodeling complex. rsc2 mutants have defects in both chromosome segregation and cohesion, but the localization of kinetochore proteins to centromeres is not affected. We determined that, in the absence of RSC2, cohesin could still associate with chromosomes but fails to achieve proper cohesion between sister chromatids, indicating that RSC has a role in the establishment of cohesion. In addition, numerous subunits of RSC were affinity purified and a new component of RSC, Rtt102, was identified. Our work indicates that only a subset of the nonessential RSC subunits function in maintaining chromosome transmission fidelity.

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Rossio, Valentina, Elena Galati, Matteo Ferrari, Achille Pellicioli, Takashi Sutani, Katsuhiko Shirahige, Giovanna Lucchini, and Simonetta Piatti. "The RSC chromatin-remodeling complex influences mitotic exit and adaptation to the spindle assembly checkpoint by controlling the Cdc14 phosphatase." Journal of Cell Biology 191, no. 5 (November 22, 2010): 981–97. http://dx.doi.org/10.1083/jcb.201007025.

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Upon prolonged activation of the spindle assembly checkpoint, cells escape from mitosis through a mechanism called adaptation or mitotic slippage, which is thought to underlie the resistance of cancer cells to antimitotic drugs. We show that, in budding yeast, this mechanism depends on known essential and nonessential regulators of mitotic exit, such as the Cdc14 early anaphase release (FEAR) pathway for the release of the Cdc14 phosphatase from the nucleolus in early anaphase. Moreover, the RSC (remodel the structure of chromatin) chromatin-remodeling complex bound to its accessory subunit Rsc2 is involved in this process as a novel component of the FEAR pathway. We show that Rsc2 interacts physically with the polo kinase Cdc5 and is required for timely phosphorylation of the Cdc14 inhibitor Net1, which is important to free Cdc14 in the active form. Our data suggest that fine-tuning regulators of mitotic exit have important functions during mitotic progression in cells treated with microtubule poisons and might be promising targets for cancer treatment.

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Hooshyar, Mohsen, Daniel Burnside, Maryam Hajikarimlou, Katayoun Omidi, Alexander Jesso, Megan Vanstone, Adamo Young, et al. "Actin-Related Protein 6 (Arp6) Influences Double-Strand Break Repair in Yeast." Applied Microbiology 1, no. 2 (July 16, 2021): 225–38. http://dx.doi.org/10.3390/applmicrobiol1020017.

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DNA double-strand breaks (DSBs) are the most deleterious form of DNA damage and are repaired through non-homologous end-joining (NHEJ) or homologous recombination (HR). Repair initiation, regulation and communication with signaling pathways require several histone-modifying and chromatin-remodeling complexes. In budding yeast, this involves three primary complexes: INO80-C, which is primarily associated with HR, SWR1-C, which promotes NHEJ, and RSC-C, which is involved in both pathways as well as the general DNA damage response. Here we identify ARP6 as a factor involved in DSB repair through an RSC-C-related pathway. The loss of ARP6 significantly reduces the NHEJ repair efficiency of linearized plasmids with cohesive ends, impairs the repair of chromosomal breaks, and sensitizes cells to DNA-damaging agents. Genetic interaction analysis indicates that ARP6, MRE11 and RSC-C function within the same pathway, and the overexpression of ARP6 rescues rsc2∆ and mre11∆ sensitivity to DNA-damaging agents. Double mutants of ARP6, and members of the INO80 and SWR1 complexes, cause a significant reduction in repair efficiency, suggesting that ARP6 functions independently of SWR1-C and INO80-C. These findings support a novel role for ARP6 in DSB repair that is independent of the SWR1 chromatin remodeling complex, through an apparent RSC-C and MRE11-associated DNA repair pathway.

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Titus, Laura C., T. Renee Dawson, Deborah J. Rexer, Kathryn J. Ryan, and Susan R. Wente. "Members of the RSC Chromatin-Remodeling Complex Are Required for Maintaining Proper Nuclear Envelope Structure and Pore Complex Localization." Molecular Biology of the Cell 21, no. 6 (March 15, 2010): 1072–87. http://dx.doi.org/10.1091/mbc.e09-07-0615.

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The assembly, distribution, and functional integrity of nuclear pore complexes (NPCs) in the nuclear envelope (NE) are key determinants in the nuclear periphery architecture. However, the mechanisms controlling proper NPC and NE structure are not fully defined. We used two different genetic screening approaches to identify Saccharomyces cerevisiae mutants with defects in NPC localization. The first approach examined green fluorescent protein (GFP)-Nic96 in 531 strains from the yeast Tet-promoters Hughes Collection with individual essential genes expressed from a doxycycline-regulated promoter (TetO7-orf). Under repressive conditions, depletion of the protein encoded by 44 TetO7-orf strains resulted in mislocalized GFP-Nic96. These included STH1, RSC4, RSC8, RSC9, RSC58, ARP7, and ARP9, each encoding components of the RSC chromatin remodeling complex. Second, a temperature-sensitive sth1-F793S (npa18-1) mutant was identified in an independent genetic screen for NPC assembly (npa) mutants. NPC mislocalization in the RSC mutants required new protein synthesis and ongoing transcription, confirming that lack of global transcription did not underlie the phenotypes. Electron microscopy studies showed significantly altered NEs and nuclear morphology, with coincident cytoplasmic membrane sheet accumulation. Strikingly, increasing membrane fluidity with benzyl alcohol treatment prevented the sth1-F793S NE structural defects and NPC mislocalization. We speculate that NE structure is functionally linked to proper chromatin architecture.

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Shim, Eun Yong, Jia-Lin Ma, Ji-Hyun Oum, Yvonne Yanez, and Sang Eun Lee. "The Yeast Chromatin Remodeler RSC Complex Facilitates End Joining Repair of DNA Double-Strand Breaks." Molecular and Cellular Biology 25, no. 10 (May 15, 2005): 3934–44. http://dx.doi.org/10.1128/mcb.25.10.3934-3944.2005.

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ABSTRACT Repair of chromosome double-strand breaks (DSBs) is central to cell survival and genome integrity. Nonhomologous end joining (NHEJ) is the major cellular repair pathway that eliminates chromosome DSBs. Here we report our genetic screen that identified Rsc8 and Rsc30, subunits of the Saccharomyces cerevisiae chromatin remodeling complex RSC, as novel NHEJ factors. Deletion of RSC30 gene or the C-terminal truncation of RSC8 impairs NHEJ of a chromosome DSB created by HO endonuclease in vivo. rsc30Δ maintains a robust level of homologous recombination and the damage-induced cell cycle checkpoints. By chromatin immunoprecipitation, we show recruitment of RSC to a chromosome DSB with kinetics congruent with its involvement in NHEJ. Recruitment of RSC to a DSB depends on Mre11, Rsc30, and yKu70 proteins. Rsc1p and Rsc2p, two other RSC subunits, physically interact with yKu80p and Mre11p. The interaction of Rsc1p with Mre11p appears to be vital for survival from genotoxic stress. These results suggest that chromatin remodeling by RSC is important for NHEJ.

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Romeo, Martin J., Melinda L. Angus-Hill, Andrew K. Sobering, Yoshiaki Kamada, Bradley R. Cairns, and David E. Levin. "HTL1 Encodes a Novel Factor That Interacts with the RSC Chromatin Remodeling Complex in Saccharomyces cerevisiae." Molecular and Cellular Biology 22, no. 23 (December 1, 2002): 8165–74. http://dx.doi.org/10.1128/mcb.22.23.8165-8174.2002.

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ABSTRACT RSC is an essential chromatin remodeling complex in Saccharomyces cerevisiae that performs central roles in transcriptional regulation and cell cycle progression. Here we identify Htl1 as a novel factor that associates with the RSC complex both physically and functionally. We isolated HTL1 through a genetic screen for mutants that displayed additive growth defects with a conditional mutation in the protein kinase C gene (PKC1), which has been suggested through genetic connections to interact functionally with RSC. Several lines of evidence connect HTL1 to RSC function. First, an htl1Δ mutant displayed temperature-sensitive growth and a G2/M cell cycle arrest at restrictive temperatures, a phenotype similar to that of strains with conditional mutations in essential RSC components. Second, we isolated RSC3, which encodes a component of the RSC complex, as a dosage suppressor of the htl1Δ growth arrest. Third, an htl1Δ mutant displayed additive growth defects with conditional rsc3 alleles. Fourth, overexpression of HTL1 suppressed the growth defect of a strain with a conditional mutation in another RSC component, RSC8. Finally, we demonstrate that Htl1 is a nuclear protein that can associate in vivo with a fraction of the RSC complex. We propose that an RSC-Htl1 complex acts coordinately with protein kinase C to regulate the G2/M transition.

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Soutourina, Julie, Véronique Bordas-Le Floch, Gabrielle Gendrel, Amando Flores, Cécile Ducrot, Hélène Dumay-Odelot, Pascal Soularue, et al. "Rsc4 Connects the Chromatin Remodeler RSC to RNA Polymerases." Molecular and Cellular Biology 26, no. 13 (July 1, 2006): 4920–33. http://dx.doi.org/10.1128/mcb.00415-06.

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ABSTRACT RSC is an essential, multisubunit chromatin remodeling complex. We show here that the Rsc4 subunit of RSC interacted via its C terminus with Rpb5, a conserved subunit shared by all three nuclear RNA polymerases (Pol). Furthermore, the RSC complex coimmunoprecipitated with all three RNA polymerases. Mutations in the C terminus of Rsc4 conferred a thermosensitive phenotype and the loss of interaction with Rpb5. Certain thermosensitive rpb5 mutations were lethal in combination with an rsc4 mutation, supporting the physiological significance of the interaction. Pol II transcription of ca. 12% of the yeast genome was increased or decreased twofold or more in a rsc4 C-terminal mutant. The transcription of the Pol III-transcribed genes SNR6 and RPR1 was also reduced, in agreement with the observed localization of RSC near many class III genes. Rsc4 C-terminal mutations did not alter the stability or assembly of the RSC complex, suggesting an impact on Rsc4 function. Strikingly, a C-terminal mutation of Rsc4 did not impair RSC recruitment to the RSC-responsive genes DUT1 and SMX3 but rather changed the chromatin accessibility of DNases to their promoter regions, suggesting that the altered transcription of DUT1 and SMX3 was the consequence of altered chromatin remodeling.

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Balachandra, Vinutha K., Jiyoti Verma, Madhu Shankar, Timothy M. Tucey, Ana Traven, Ralf B. Schittenhelm, and Santanu K. Ghosh. "The RSC (Remodels the Structure of Chromatin) complex of Candida albicans shows compositional divergence with distinct roles in regulating pathogenic traits." PLOS Genetics 16, no. 11 (November 5, 2020): e1009071. http://dx.doi.org/10.1371/journal.pgen.1009071.

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Regulation of gene expression programs is crucial for the survival of microbial pathogens in host environments and for their ability to cause disease. Here we investigated the epigenetic regulator RSC (Remodels the Structure of Chromatin) in the most prevalent human fungal pathogen Candida albicans. Biochemical analysis showed that CaRSC comprises 13 subunits and contains two novel non-essential members, which we named Nri1 and Nri2 (Novel RSC Interactors) that are exclusive to the CTG clade of Saccharomycotina. Genetic analysis showed distinct essentiality of C. albicans RSC subunits compared to model fungal species suggesting functional and structural divergence of RSC functions in this fungal pathogen. Transcriptomic and proteomic profiling of a conditional mutant of the essential catalytic subunit gene STH1 demonstrated global roles of RSC in C. albicans biology, with the majority of growth-related processes affected, as well as mis-regulation of genes involved in morphotype switching, host-pathogen interaction and adaptive fitness. We further assessed the functions of non-essential CaRSC subunits, showing that the novel subunit Nri1 and the bromodomain subunit Rsc4 play roles in filamentation and stress responses; and also interacted at the genetic level to regulate cell viability. Consistent with these roles, Rsc4 is required for full virulence of C. albicans in the murine model of systemic infection. Taken together, our data builds the first comprehensive study of the composition and roles of RSC in C. albicans, showing both conserved and distinct features compared to model fungal systems. The study illuminates how C. albicans uses RSC-dependent transcriptional regulation to respond to environmental signals and drive survival fitness and virulence in mammals.

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Kent, Nicholas A., Anna L. Chambers, and Jessica A. Downs. "Dual Chromatin Remodeling Roles for RSC during DNA Double Strand Break Induction and Repair at the Yeast MAT Locus." Journal of Biological Chemistry 282, no. 38 (July 25, 2007): 27693–701. http://dx.doi.org/10.1074/jbc.m704707200.

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DNA double strand breaks (DSBs) are potentially serious chromosomal lesions. However, cells sometimes deliberately cleave their own DNA to facilitate certain chromosomal processes, and there is much interest in how such self-inflicted breaks are effectively managed. Eukaryotic DSBs occur in the context of chromatin and the RSC chromatin-remodeling ATPase complex has been shown to promote DSB repair at the budding yeast MAT locus DSB, created by the HO endonuclease during mating type switching. We show that the role of RSC at MAT is highly specialized. The Rsc1p subunit of RSC directs nucleosome sliding immediately after DSB creation at both MAT and generally and is required for efficient DNA damage-induced histone H2A phosphorylation and strand resection during repair by homologous recombination. However, the Rsc2p and Rsc7p subunits are additionally required to set up a basal MAT locus structure. This RSC-dependent chromatin structure at MAT ensures accessibility to the HO endonuclease. The RSC complex therefore has chromatin remodeling roles both before and after DSB induction at MAT, promoting both DNA cleavage and subsequent repair.

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Damelin, Marc, Itamar Simon, Terence I. Moy, Boris Wilson, Suzanne Komili, Paul Tempst, Frederick P. Roth, Richard A. Young, Bradley R. Cairns, and Pamela A. Silver. "The Genome-Wide Localization of Rsc9, a Component of the RSC Chromatin-Remodeling Complex, Changes in Response to Stress." Molecular Cell 9, no. 3 (March 2002): 563–73. http://dx.doi.org/10.1016/s1097-2765(02)00475-6.

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Sanz, Ana Belén, Sonia Díez-Muñiz, Jennifer Moya, Yuliya Petryk, César Nombela, José M. Rodríguez-Peña, and Javier Arroyo. "Systematic Identification of Essential Genes Required for Yeast Cell Wall Integrity: Involvement of the RSC Remodelling Complex." Journal of Fungi 8, no. 7 (July 8, 2022): 718. http://dx.doi.org/10.3390/jof8070718.

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Conditions altering the yeast cell wall lead to the activation of an adaptive transcriptional response mainly governed by the cell wall integrity (CWI) mitogen-activated protein kinase (MAPK) pathway. Two high-throughput screenings were developed using the yTHC collection of yeast conditional mutant strains to systematically identify essential genes related to cell wall integrity, and those required for the transcriptional program elicited by cell wall stress. Depleted expression of 52 essential genes resulted in hypersensitivity to the dye Calcofluor white, with chromatin organization, Golgi vesicle transport, rRNA processing, and protein glycosylation processes, as the most highly representative functional groups. Via a flow cytometry-based quantitative assay using a CWI reporter plasmid, 97 strains exhibiting reduced gene-reporter expression levels upon stress were uncovered, highlighting genes associated with RNA metabolism, transcription/translation, protein degradation, and chromatin organization. This screening also led to the discovery of 41 strains displaying a basal increase in CWI-associated gene expression, including mainly putative cell wall-related genes. Interestingly, several members of the RSC chromatin remodelling complex were uncovered in both screenings. Notably, Rsc9 was necessary to regulate the gene expression of CWI-related genes both under stress and non-stress conditions, suggesting distinct requirements of the RSC complex for remodelling particular genes.

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Campsteijn, Coen, Anne-Marie J. Wijnands-Collin, and Colin Logie. "Reverse Genetic Analysis of Yeast RSC Chromatin Remodeling Complex Subunits Reveals a Role for RSC3 and SNF5 Homologue 1 in Ploidy Maintenance." PLoS Genetics preprint, no. 2007 (2005): e92. http://dx.doi.org/10.1371/journal.pgen.0030092.eor.

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Concas, Maria Pina, Anna Morgan, Paola Tesolin, Aurora Santin, Giorgia Girotto, and Paolo Gasparini. "Sensory Capacities and Eating Behavior: Intriguing Results from a Large Cohort of Italian Individuals." Foods 11, no. 5 (March 2, 2022): 735. http://dx.doi.org/10.3390/foods11050735.

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Eating behavior (EB) is a complex system influenced by many factors, but an undisputed role is played by the senses. In this work, we examined the effect of the sensory capacities on EB in 1152 Italian adult individuals. After administering a questionnaire on EB and assessing sensory performance through standard audiometric, olfactory, and taste tests, the prevalence of reduced sensory capacities (RSCs) and the correlation with selected risk factors were calculated. Regression models, structural equation modelling, and conditional recursive partitioning were used to investigate the relationship between variables. Around 70% of the subjects show reduced capacities in at least one sense, with taste being the most prevalent (55.21%). Male sex, aging, and low educational level are risk factors for RSCs. The increased number of senses with reduced capacities is a predictor of diminished food adventurousness and lower liking for vegetables, fish, and alcoholic beverages, while reduced capacities (RCs) in taste is a predictor of lower liking for alcoholic beverages and sweets. Overall, in addition to providing an overall picture of RSCs in Italian samples, our study reveals the association of RSCs with EB variables. This finding could have a relevant role in influencing individuals’ dietary habits and, therefore, health status.

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Ljubotina, Predrag. "The influence of entrepreneurial skills, education and risk perception on career choice intent: The case of European students with family business background." Research in Social Change 12, no. 1 (January 1, 2020): 23–37. http://dx.doi.org/10.2478/rsc-2020-0002.

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Abstract When confronted with career choice, students with family business background have a specific trilemma. Having an additional career alternative as a potential family business successor, makes their career choice decision more complex compared with their peers. The purpose of this paper is to investigate how entrepreneurial education, risk perception and skill mastering influence career choice intention of this specific group of students. We used a data set from GUESSS 2014 survey. Our sample includes students with family business background from 18 European countries. We used a multinomial logistic regression since our dependant variable has three categorical solutions (entrepreneur, employee and successor). Our findings may be used by consultants, education institutions and more importantly by parents which find themselves in a triple role of an entrepreneur, an owner and a parent.

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Bareiro, Diego, Enrique O’Durnin, Laura Oporto, and Christian Schaerer. "Shallow water model for pollutant distribution in the Ypacarai Lake." Revista de la Sociedad Científica del Paraguay 26, no. 2 (November 30, 2021): 54–76. http://dx.doi.org/10.32480/rscp.2021.26.2.54.

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In this paper, we analyze the distribution of a non-reactive contaminant in Ypacarai Lake. We propose a shallow-water model that considers wind-induced currents, inflow and outflow conditions in the tributaries, and bottom effects due to the lakebed. The hydrodynamic is based on the depth-averaged Navier-Stokes equations considering wind stresses as force terms which are functions of the wind velocity. Bed (bottom) stress is based on Manning's equation, the lakebed characteristics, and wind velocities. The contaminant transportation is modeled by a 2D convection-diffusion equation taking into consideration water level. Comparisons between the simulation of the model, analytical solutions, and laboratory results confirm that the model captures the complex dynamic phenomenology of the lake. In the simulations, one can see the regions with the highest risk of accumulation of contaminants. It is observed the effect of each term and how it can be used them to mitigate the impact of the pollutants.

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Ndreka, Alkida. "Return migration and re-integration of returnees challenges in the origin country." Research in Social Change 11, no. 3 (September 1, 2019): 4–24. http://dx.doi.org/10.2478/rsc-2019-0012.

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Abstract Return migration, traditionally not a well-studied and often neglected area, is becoming an important component of the international migration debate. Reintegration is an essential part of return migration and identified as a complex process that is experienced differently by returnees. The adaptation of immigrants in the host country has been extensively studied, while much less attention has been paid to economic and socio-cultural reintegration and the difficulties return migrants face once they come back to their homeland. Especially children and youth born in destination countries with sociolinguistic and socialization difficulties face a particularly tough reintegration process. Theoretically, there is comprehensive literature focused on return migration and reasons for return, but less in return migration policies and reintegration process. Empirically, there is a lack of studies focused on the reintegration of returnees, particularly in the socio-cultural aspect. With increased attention to the importance of this process, many states and governments have established policies or programs to encourage the return of their citizens, and facilitate returnees’ successful and permanent relocation in the new society of the origin country. This paper aims to analyze theoretically and empirically the processes of reintegration of returnees in the origin country by identifying the challenges they encounter in the economic and social-cultural life of the origin country.

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Yu, Feifei, Yuko Imamura, Masaru Ueno, Sho W. Suzuki, Yoshinori Ohsumi, Masashi Yukawa, and Eiko Tsuchiya. "The yeast chromatin remodeler Rsc1-RSC complex is required for transcriptional activation of autophagy-related genes and inhibition of the TORC1 pathway in response to nitrogen starvation." Biochemical and Biophysical Research Communications 464, no. 4 (September 2015): 1248–53. http://dx.doi.org/10.1016/j.bbrc.2015.07.114.

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Schlichter, Alisha, Margaret M. Kasten, Timothy J. Parnell, and Bradley R. Cairns. "Specialization of the chromatin remodeler RSC to mobilize partially-unwrapped nucleosomes." eLife 9 (June 4, 2020). http://dx.doi.org/10.7554/elife.58130.

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SWI/SNF-family chromatin remodeling complexes, such as S. cerevisiae RSC, slide and eject nucleosomes to regulate transcription. Within nucleosomes, stiff DNA sequences confer spontaneous partial unwrapping, prompting whether and how SWI/SNF-family remodelers are specialized to remodel partially-unwrapped nucleosomes. RSC1 and RSC2 are orthologs of mammalian PBRM1 (polybromo) which define two separate RSC sub-complexes. Remarkably, in vitro the Rsc1-containing complex remodels partially-unwrapped nucleosomes much better than does the Rsc2-containing complex. Moreover, a rsc1Δ mutation, but not rsc2Δ, is lethal with histone mutations that confer partial unwrapping. Rsc1/2 isoforms both cooperate with the DNA-binding proteins Rsc3/30 and the HMG protein, Hmo1, to remodel partially-unwrapped nucleosomes, but show differential reliance on these factors. Notably, genetic impairment of these factors strongly reduces the expression of genes with wide nucleosome-deficient regions (e.g., ribosomal protein genes), known to harbor partially-unwrapped nucleosomes. Taken together, Rsc1/2 isoforms are specialized through composition and interactions to manage and remodel partially-unwrapped nucleosomes.

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Patel, Avinash B., Camille M. Moore, Basil J. Greber, Jie Luo, Stefan A. Zukin, Jeff Ranish, and Eva Nogales. "Architecture of the chromatin remodeler RSC and insights into its nucleosome engagement." eLife 8 (December 30, 2019). http://dx.doi.org/10.7554/elife.54449.

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Eukaryotic DNA is packaged into nucleosome arrays, which are repositioned by chromatin remodeling complexes to control DNA accessibility. The Saccharomyces cerevisiae RSC (Remodeling the Structure of Chromatin) complex, a member of the SWI/SNF chromatin remodeler family, plays critical roles in genome maintenance, transcription, and DNA repair. Here, we report cryo-electron microscopy (cryo-EM) and crosslinking mass spectrometry (CLMS) studies of yeast RSC complex and show that RSC is composed of a rigid tripartite core and two flexible lobes. The core structure is scaffolded by an asymmetric Rsc8 dimer and built with the evolutionarily conserved subunits Sfh1, Rsc6, Rsc9 and Sth1. The flexible ATPase lobe, composed of helicase subunit Sth1, Arp7, Arp9 and Rtt102, is anchored to this core by the N-terminus of Sth1. Our cryo-EM analysis of RSC bound to a nucleosome core particle shows that in addition to the expected nucleosome-Sth1 interactions, RSC engages histones and nucleosomal DNA through one arm of the core structure, composed of the Rsc8 SWIRM domains, Sfh1 and Npl6. Our findings provide structural insights into the conserved assembly process for all members of the SWI/SNF family of remodelers, and illustrate how RSC selects, engages, and remodels nucleosomes.

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Navasa, Nicolás, Leandro Rodríguez-Aparicio, Miguel Ángel Ferrero, Andrea Monteagudo-Mera, and Honorina Martínez-Blanco. "Polysialic and colanic acids metabolism in Escherichia coli K92 is regulated by RcsA and RcsB." Bioscience Reports 33, no. 3 (May 24, 2013). http://dx.doi.org/10.1042/bsr20130018.

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We have shown previously that Escherichia coli K92 produces two different capsular polymers known as CA (colanic acid) and PA (polysialic acid) in a thermoregulated manner. The complex Rcs phosphorelay is largely related to the regulation of CA synthesis. Through deletion of rscA and rscB genes, we show that the Rcs system is involved in the regulation of both CA and PA synthesis in E. coli K92. Deletion of either rcsA or rcsB genes resulted in decreased expression of cps (CA biosynthesis cluster) at 19°C and 37°C, but only CA production was reduced at 19°C. Concerning PA, both deletions enhanced its synthesis at 37°C, which does not correlate with the reduced kps (PA biosynthesis cluster) expression observed in the rcsB mutant. Under this condition, expression of the nan operon responsible for PA catabolism was greatly reduced. Although RcsA and RcsB acted as negative regulators of PA synthesis at 37°C, their absence did not reestablish PA expression at low temperatures, despite the deletion of rcsB resulting in enhanced kps expression. Finally, our results revealed that RcsB controlled the expression of several genes (dsrA, rfaH, h-ns and slyA) involved in the thermoregulation of CA and PA synthesis, indicating that RcsB is part of a complex regulatory mechanism governing the surface appearance in E. coli.

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Locci, Emanuela. "The Masonic Degree of Rose-Croix and Christianity: The Complex Links between Religion and Freemasonry during the Enlightenment." Ritual, Secrecy, and Civil Society, 2013. http://dx.doi.org/10.18278/rscs.1.2.2.

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Yuan, Huiling, Ying Zhou, Yuping Lin, Ran Tu, Yufeng Guo, Yuanyuan Zhang, and Qinhong Wang. "Microfluidic screening and genomic mutation identification for enhancing cellulase production in Pichia pastoris." Biotechnology for Biofuels and Bioproducts 15, no. 1 (May 14, 2022). http://dx.doi.org/10.1186/s13068-022-02150-w.

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Abstract Background Pichia pastoris is a widely used host organism for heterologous production of industrial proteins, such as cellulases. Although great progress has been achieved in improving protein expression in P. pastoris, the potential of the P. pastoris expression system has not been fully explored due to unknown genomic impact factors. Recently, whole-cell directed evolution, employing iterative rounds of genome-wide diversity generation and high-throughput screening (HTS), has been considered to be a promising strategy in strain improvement at the genome level. Results In this study, whole-cell directed evolution of P. pastoris, employing atmospheric and room temperature plasma (ARTP) mutagenesis and droplet-based microfluidic HTS, was developed to improve heterogenous cellulase production. The droplet-based microfluidic platform based on a cellulase-catalyzed reaction of releasing fluorescence was established to be suitable for methanol-grown P. pastoris. The validation experiment showed a positive sorting efficiency of 94.4% at a sorting rate of 300 droplets per second. After five rounds of iterative ARTP mutagenesis and microfluidic screening, the best mutant strain was obtained and exhibited the cellulase activity of 11,110 ± 523 U/mL, an approximately twofold increase compared to the starting strain. Whole-genome resequencing analysis further uncovered three accumulated genomic alterations in coding region. The effects of point mutations and mutant genes on cellulase production were verified using reconstruction of point mutations and gene deletions. Intriguingly, the point mutation Rsc1G22V was observed in all the top-performing producers selected from each round, and gene deletion analysis confirmed that Rsc1, a component of the RSC chromatin remodeling complex, might play an important role in cellulase production. Conclusions We established a droplet-based microfluidic HTS system, thereby facilitating whole-cell directed evolution of P. pastoris for enhancing cellulase production, and meanwhile identified genomic alterations by whole-genome resequencing and genetic validation. Our approaches and findings would provide guides to accelerate whole-cell directed evolution of host strains and enzymes of high industrial interest.

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Journal articles on the topic 'RSC complex, Rsc2'

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