Journal articles: 'Genetic transcription'

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NOMURA, Teruaki, and Akira ISHIHAMA. "Transcription regulation of genetic information. Properties of transcriptional signals." Kagaku To Seibutsu 23, no. 10 (1985): 632–39. http://dx.doi.org/10.1271/kagakutoseibutsu1962.23.632.

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Guo, Shaobin, Zeqi Xu, Lujie Lin, Yan Guo, Jingying Li, Chunhua Lu, Xianai Shi, and Huanghao Yang. "Using CIVT-SELEX to Select Aptamers as Genetic Parts to Regulate Gene Circuits in a Cell-Free System." International Journal of Molecular Sciences 24, no. 3 (February 1, 2023): 2833. http://dx.doi.org/10.3390/ijms24032833.

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The complexity of genetic circuits has not seen a significant increase over the last decades, even with the rapid development of synthetic biology tools. One of the bottlenecks is the limited number of orthogonal transcription factor–operator pairs. Researchers have tried to use aptamer–ligand pairs as genetic parts to regulate transcription. However, most aptamers selected using traditional methods cannot be directly applied in gene circuits for transcriptional regulation. To that end, we report a new method called CIVT-SELEX to select DNA aptamers that can not only bind to macromolecule ligands but also undergo significant conformational changes, thus affecting transcription. The single-stranded DNA library with affinity to our example ligand human thrombin protein is first selected and enriched. Then, these ssDNAs are inserted into a genetic circuit and tested in the in vitro transcription screening to obtain the ones with significant inhibitory effects on downstream gene transcription when thrombins are present. These aptamer–thrombin pairs can inhibit the transcription of downstream genes, demonstrating the feasibility and robustness of their use as genetic parts in both linear DNAs and plasmids. We believe that this method can be applied to select aptamers of any target ligands and vastly expand the genetic part library for transcriptional regulation.

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Wang, R., E. Halper-Stromberg, M. Szymanski-Pierce, S. S. Bassett, and D. Avramopoulos. "Genetic determinants of neuroglobin transcription." neurogenetics 15, no. 1 (December 24, 2013): 65–75. http://dx.doi.org/10.1007/s10048-013-0388-3.

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Chua, Gordon. "Systematic genetic analysis of transcription factors to map the fission yeast transcription-regulatory network." Biochemical Society Transactions 41, no. 6 (November 20, 2013): 1696–700. http://dx.doi.org/10.1042/bst20130224.

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Mapping transcriptional-regulatory networks requires the identification of target genes, binding specificities and signalling pathways of transcription factors. However, the characterization of each transcription factor sufficiently for deciphering such networks remains laborious. The recent availability of overexpression and deletion strains for almost all of the transcription factor genes in the fission yeast Schizosaccharomyces pombe provides a valuable resource to better investigate transcription factors using systematic genetics. In the present paper, I review and discuss the utility of these strain collections combined with transcriptome profiling and genome-wide chromatin immunoprecipitation to identify the target genes of transcription factors.

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Sansó, Miriam, and Robert P. Fisher. "Modelling the CDK-dependent transcription cycle in fission yeast." Biochemical Society Transactions 41, no. 6 (November 20, 2013): 1660–65. http://dx.doi.org/10.1042/bst20130238.

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CDKs (cyclin-dependent kinases) ensure directionality and fidelity of the eukaryotic cell division cycle. In a similar fashion, the transcription cycle is governed by a conserved subfamily of CDKs that phosphorylate Pol II (RNA polymerase II) and other substrates. A genetic model organism, the fission yeast Schizosaccharomyces pombe, has yielded robust models of cell-cycle control, applicable to higher eukaryotes. From a similar approach combining classical and chemical genetics, fundamental principles of transcriptional regulation by CDKs are now emerging. In the present paper, we review the current knowledge of each transcriptional CDK with respect to its substrate specificity, function in transcription and effects on chromatin modifications, highlighting the important roles of CDKs in ensuring quantity and quality control over gene expression in eukaryotes.

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Newton, A., N. Ohta, G. Ramakrishnan, D. Mullin, and G. Raymond. "Genetic switching in the flagellar gene hierarchy of Caulobacter requires negative as well as positive regulation of transcription." Proceedings of the National Academy of Sciences 86, no. 17 (September 1989): 6651–55. http://dx.doi.org/10.1073/pnas.86.17.6651.

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Caulobacter crescentus flagellar (fla, flb, or flg) genes are periodically expressed in the cell cycle and they are organized in a regulatory hierarchy. We have analyzed the genetic interactions required for fla gene expression by determining the effect of mutations in 30 known fla genes on transcription from four operons in the hook gene cluster. These results show that the flaO (transcription unit III) and flbF (transcription unit IV) operons are located at or near the top of the hierarchy. They also reveal an extensive network of negative transcriptional controls that are superimposed on the positive regulatory cascade described previously. The strong negative autoregulation observed for the flaN (transcription unit I), flbG (transcription unit II), and flaO (transcription unit III) promoters provides one possible mechanism for turning off fla gene expression at the end of the respective synthetic periods. We suggest that these positive and negative transcriptional interactions are components of genetic switches that determine the sequence in which fla genes are turned on and off in the C. crescentus cell cycle.

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Fazlollahi, Mina, Ivor Muroff, Eunjee Lee, Helen C. Causton, and Harmen J. Bussemaker. "Identifying genetic modulators of the connectivity between transcription factors and their transcriptional targets." Proceedings of the National Academy of Sciences 113, no. 13 (March 10, 2016): E1835—E1843. http://dx.doi.org/10.1073/pnas.1517140113.

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Regulation of gene expression by transcription factors (TFs) is highly dependent on genetic background and interactions with cofactors. Identifying specific context factors is a major challenge that requires new approaches. Here we show that exploiting natural variation is a potent strategy for probing functional interactions within gene regulatory networks. We developed an algorithm to identify genetic polymorphisms that modulate the regulatory connectivity between specific transcription factors and their target genes in vivo. As a proof of principle, we mapped connectivity quantitative trait loci (cQTLs) using parallel genotype and gene expression data for segregants from a cross between two strains of the yeast Saccharomyces cerevisiae. We identified a nonsynonymous mutation in the DIG2 gene as a cQTL for the transcription factor Ste12p and confirmed this prediction empirically. We also identified three polymorphisms in TAF13 as putative modulators of regulation by Gcn4p. Our method has potential for revealing how genetic differences among individuals influence gene regulatory networks in any organism for which gene expression and genotype data are available along with information on binding preferences for transcription factors.

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Frank, Steven A. "Optimization of Transcription Factor Genetic Circuits." Biology 11, no. 9 (August 31, 2022): 1294. http://dx.doi.org/10.3390/biology11091294.

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Transcription factors (TFs) affect the production of mRNAs. In essence, the TFs form a large computational network that controls many aspects of cellular function. This article introduces a computational method to optimize TF networks. The method extends recent advances in artificial neural network optimization. In a simple example, computational optimization discovers a four-dimensional TF network that maintains a circadian rhythm over many days, successfully buffering strong stochastic perturbations in molecular dynamics and entraining to an external day–night signal that randomly turns on and off at intervals of several days. This work highlights the similar challenges in understanding how computational TF and neural networks gain information and improve performance.

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Drazen, Jeffrey M., and Eric S. Silverman. "Genetic Determinants of 5–Lipoxygenase Transcription." International Archives of Allergy and Immunology 118, no. 2-4 (1999): 275–78. http://dx.doi.org/10.1159/000024098.

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Seo, Young Jun, Shigeo Matsuda, and Floyd E. Romesberg. "Transcription of an Expanded Genetic Alphabet." Journal of the American Chemical Society 131, no. 14 (April 15, 2009): 5046–47. http://dx.doi.org/10.1021/ja9006996.

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Ibrahim, Lara, Jaleh Mesgarzadeh, Ian Xu, Evan T. Powers, R. Luke Wiseman, and Michael J. Bollong. "Defining the Functional Targets of Cap‘n’collar Transcription Factors NRF1, NRF2, and NRF3." Antioxidants 9, no. 10 (October 21, 2020): 1025. http://dx.doi.org/10.3390/antiox9101025.

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The NRF transcription factors NRF1, NRF2, and NRF3, are a subset of Cap‘n’collar transcriptional regulators which modulate the expression of genes harboring antioxidant-response element (ARE) sequences within their genomic loci. Despite the emerging physiological importance of NRF family members, the repertoire of their genetic targets remains incompletely defined. Here we use RNA-sequencing-based transcriptional profiling and quantitative proteomics to delineate the overlapping and differential genetic programs effected by the three NRF transcription factors. We then create consensus target gene sets regulated by NRF1, NRF2, and NRF3 and define the integrity of these gene sets for probing NRF activity in mammalian cell culture and human tissues. Together, our data provide a quantitative assessment of how NRF family members sculpt proteomes and transcriptomes, providing a framework to understand the critical physiological importance of NRF transcription factors and to establish pharmacologic approaches for therapeutically activating these transcriptional programs in disease.

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Leal, Nicole A., Hyo-Joong Kim, Shuichi Hoshika, Myong-Jung Kim, Matthew A. Carrigan, and Steven A. Benner. "Transcription, Reverse Transcription, and Analysis of RNA Containing Artificial Genetic Components." ACS Synthetic Biology 4, no. 4 (August 19, 2014): 407–13. http://dx.doi.org/10.1021/sb500268n.

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Smith, H. E., S. E. Driscoll, R. A. Sia, H. E. Yuan, and A. P. Mitchell. "Genetic evidence for transcriptional activation by the yeast IME1 gene product." Genetics 133, no. 4 (April 1, 1993): 775–84. http://dx.doi.org/10.1093/genetics/133.4.775.

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Abstract IME1 is required in yeast for meiosis and for expression of IME2 and other early meiotic genes. IME1 is a 360-amino acid polypeptide with central and C-terminal tyrosine-rich regions. We report here that a fusion protein composed of the lexA DNA-binding domain and IME1 activates transcription in vivo of a reporter gene containing upstream lexA binding sites. Activation by the fusion protein shares several features with natural IME1 activity: both are dependent on the RIM11 gene product; both are impaired by the same ime1 missense mutations; both are restored by intragenic suppressors. The central tyrosine-rich region is sufficient to activate transcription when fused to lexA. Deletion of this putative activation domain results in a defective IME1 derivative. Function of the deletion derivative is restored by fusion to the acidic Herpesvirus VP16 activation domain. The C-terminal tyrosine-rich region is dispensable for transcriptional activation; rather it renders activation dependent upon starvation and RIM11. Immunofluorescence studies indicate that an IME1-lacZ fusion protein is concentrated in the nucleus. These observations are consistent with a model in which IME1 normally stimulates IME2 expression by providing a transcriptional activation domain at the IME2 5' regulatory region.

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Morey, Natalie J., Christopher N. Greene, and Sue Jinks-Robertson. "Genetic Analysis of Transcription-Associated Mutation in Saccharomyces cerevisiae." Genetics 154, no. 1 (January 1, 2000): 109–20. http://dx.doi.org/10.1093/genetics/154.1.109.

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Abstract High levels of transcription are associated with elevated mutation rates in yeast, a phenomenon referred to as transcription-associated mutation (TAM). The transcription-associated increase in mutation rates was previously shown to be partially dependent on the Rev3p translesion bypass pathway, thus implicating DNA damage in TAM. In this study, we use reversion of a pGAL-driven lys2ΔBgl allele to further examine the genetic requirements of TAM. We find that TAM is increased by disruption of the nucleotide excision repair or recombination pathways. In contrast, elimination of base excision repair components has only modest effects on TAM. In addition to the genetic studies, the lys2ΔBgl reversion spectra of repair-proficient low and high transcription strains were obtained. In the low transcription spectrum, most of the frameshift events correspond to deletions of AT base pairs whereas in the high transcription strain, deletions of GC base pairs predominate. These results are discussed in terms of transcription and its role in DNA damage and repair.

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Chan, J. Y., X. L. Han, and Y. W. Kan. "Cloning of Nrf1, an NF-E2-related transcription factor, by genetic selection in yeast." Proceedings of the National Academy of Sciences 90, no. 23 (December 1, 1993): 11371–75. http://dx.doi.org/10.1073/pnas.90.23.11371.

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We have devised a complementation assay in yeast to clone mammalian transcriptional activators and have used it to identify a human basic leucine-zipper transcription factor that we have designated Nrf1 for NF-E2-related factor 1. Nrf1 potentially encodes a 742-aa protein and displays marked homology to the mouse and human NF-E2 transcription factors. Nrf1 activates transcription via NF-E2 binding sites in yeast cells. The ubiquitous expression pattern of Nrf1 and the range of promoters containing the NF-E2 binding motif suggest that this gene may play a role in the regulation of heme synthesis and ferritin genes.

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Lee, Young Chul, and Young-Joon Kim. "Requirement for a Functional Interaction between Mediator Components Med6 and Srb4 in RNA Polymerase II Transcription." Molecular and Cellular Biology 18, no. 9 (September 1, 1998): 5364–70. http://dx.doi.org/10.1128/mcb.18.9.5364.

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ABSTRACT Regulated transcription of class II genes of the yeastSaccharomyces cerevisiae requires the diverse functions of mediator complex. In particular, MED6 is essential for activated transcription from many class II promoters, suggesting that it functions as a key player in the relay of activator signals to the basal transcription machinery. To identify the functional relationship between MED6 and other transcriptional regulators, we conducted a genetic screen to isolate a suppressor of a temperature-sensitive (ts) med6 mutation. We identified an SRB4 allele as a dominant and allele-specific suppressor of med6-ts. A single missense mutation inSRB4 can specifically suppress transcriptional defects caused by the med6 ts mutation, indicating a functional interaction between these two mediator subunits in the activation of transcription. Biochemical analysis of mediator subassembly revealed that mediator can be dissociated into two tightly associated subcomplexes. The Med6 and Srb4 proteins are contained in the same subcomplex together with other dominant Srb proteins, consistent with their functional relationship revealed by the genetic study. Our results suggest not only the existence of a specific interaction between Med6 and Srb4 but also the requirement of this interaction in transcriptional regulation of RNA polymerase II holoenzyme.

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Jenkins, Dafyd J., and Dov J. Stekel. "A New Model for Investigating the Evolution of Transcription Control Networks." Artificial Life 15, no. 3 (July 2009): 259–91. http://dx.doi.org/10.1162/artl.2009.stekel.006.

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Biological systems show unbounded capacity for complex behaviors and responses to their environments. This principally arises from their genetic networks. The processes governing transcription, translation, and gene regulation are well understood, as are the mechanisms of network evolution, such as gene duplication and horizontal gene transfer. However, the evolved networks arising from these simple processes are much more difficult to understand, and it is difficult to perform experiments on the evolution of these networks in living organisms because of the timescales involved. We propose a new framework for modeling and investigating the evolution of transcription networks in realistic, varied environments. The model we introduce contains novel, important, and lifelike features that allow the evolution of arbitrarily complex transcription networks. Molecular interactions are not specified; instead they are determined dynamically based on shape, allowing protein function to freely evolve. Transcriptional logic provides a flexible mechanism for defining genetic regulatory activity. Simulations demonstrate a realistic life cycle as an emergent property, and that even in simple environments lifelike and complex regulation mechanisms are evolved, including stable proteins, unstable mRNA, and repressor activity. This study also highlights the importance of using in silico genetics techniques to investigate evolved model robustness.

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Dorland, Scott, Michelle L. Deegenaars, and David J. Stillman. "Roles for the Saccharomyces cerevisiae SDS3, CBK1 and HYM1 Genes in Transcriptional Repression by SIN3." Genetics 154, no. 2 (February 1, 2000): 573–86. http://dx.doi.org/10.1093/genetics/154.2.573.

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Abstract The Saccharomyces cerevisiae Sin3 transcriptional repressor is part of a large multiprotein complex that includes the Rpd3 histone deacetylase. A LexA-Sin3 fusion protein represses transcription of promoters with LexA binding sites. To identify genes involved in repression by Sin3, we conducted a screen for mutations that reduce repression by LexA-Sin3. One of the mutations identified that reduces LexA-Sin3 repression is in the RPD3 gene, consistent with the known roles of Rpd3 in transcriptional repression. Mutations in CBK1 and HYM1 reduce repression by LexA-Sin3 and also cause defects in cell separation and altered colony morphology. cbk1 and hym1 mutations affect some but not all genes regulated by SIN3 and RPD3, but the effect on transcription is much weaker. Genetic analysis suggests that CBK1 and HYM1 function in the same pathway, but this genetic pathway is separable from that of SIN3 and RPD3. The remaining gene from this screen described in this report is SDS3, previously identified in a screen for mutations that increase silencing at HML, HMR, and telomere-linked genes, a phenotype also seen in sin3 and rpd3 mutants. Genetic analysis demonstrates that SDS3 functions in the same genetic pathway as SIN3 and RPD3, and coimmunoprecipitation experiments show that Sds3 is physically present in the Sin3 complex.

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Zhu, Qian, Xavier Tekpli, Olga G. Troyanskaya, and Vessela N. Kristensen. "Subtype-specific transcriptional regulators in breast tumors subjected to genetic and epigenetic alterations." Bioinformatics 36, no. 4 (September 16, 2019): 994–99. http://dx.doi.org/10.1093/bioinformatics/btz709.

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Abstract Motivation Breast cancer consists of multiple distinct tumor subtypes, and results from epigenetic and genetic aberrations that give rise to distinct transcriptional profiles. Despite previous efforts to understand transcriptional deregulation through transcription factor networks, the transcriptional mechanisms leading to subtypes of the disease remain poorly understood. Results We used a sophisticated computational search of thousands of expression datasets to define extended signatures of distinct breast cancer subtypes. Using ENCODE ChIP-seq data of surrogate cell lines and motif analysis we observed that these subtypes are determined by a distinct repertoire of lineage-specific transcription factors. Furthermore, specific pattern and abundance of copy number and DNA methylation changes at these TFs and targets, compared to other genes and to normal cells were observed. Overall, distinct transcriptional profiles are linked to genetic and epigenetic alterations at lineage-specific transcriptional regulators in breast cancer subtypes. Availability and implementation The analysis code and data are deposited at https://bitbucket.org/qzhu/breast.cancer.tf/. Supplementary information Supplementary data are available at Bioinformatics online.

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Braun, Christian J., Peter M. Bruno, Max A. Horlbeck, Luke A. Gilbert, Jonathan S. Weissman, and Michael T. Hemann. "Versatile in vivo regulation of tumor phenotypes by dCas9-mediated transcriptional perturbation." Proceedings of the National Academy of Sciences 113, no. 27 (June 20, 2016): E3892—E3900. http://dx.doi.org/10.1073/pnas.1600582113.

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Targeted transcriptional regulation is a powerful tool to study genetic mediators of cellular behavior. Here, we show that catalytically dead Cas9 (dCas9) targeted to genomic regions upstream or downstream of the transcription start site allows for specific and sustainable gene-expression level alterations in tumor cells in vitro and in syngeneic immune-competent mouse models. We used this approach for a high-coverage pooled gene-activation screen in vivo and discovered previously unidentified modulators of tumor growth and therapeutic response. Moreover, by using dCas9 linked to an activation domain, we can either enhance or suppress target gene expression simply by changing the genetic location of dCas9 binding relative to the transcription start site. We demonstrate that these directed changes in gene-transcription levels occur with minimal off-target effects. Our findings highlight the use of dCas9-mediated transcriptional regulation as a versatile tool to reproducibly interrogate tumor phenotypes in vivo.

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Forbes, A. J., Y. Nakano, A. M. Taylor, and P. W. Ingham. "Genetic analysis of hedgehog signalling in the Drosophila embryo." Development 119, Supplement (December 1, 1993): 115–24. http://dx.doi.org/10.1242/dev.119.supplement.115.

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The segment polarity genes play a fundamental role in the patterning of cells within individual body segments of the Drosophila embryo. Two of these genes wingless (wg) and hedgehog (hh) encode proteins that enter the secretory pathway and both are thought to act by instructing the fates of cells neighbouring those in which they are expressed. Genetic analysis bas identified the transcriptional activation of wg as one of the targets of hh activity: here we present evidence that transduction of the hh-encoded signal is mediated by the activity of four other segment polarity genes, patched, fused, costal-2 and cubitus interruptus. The results of our genetic epistatsis analysis together with the molecular structures of the products of these genes where known, suggest a pathway of interactions leading from reception of the hh-encoded signal at the cell membrane to transcriptional activation in the cell nucleus. We have also found that transcription of patched is regulated by the same pathway and describe the identification of cis-acting upstream elements of the ptc transcription unit that mediate this regulation.

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Basu, Urmimala, Alicia M. Bostwick, Kalyan Das, Kristin E. Dittenhafer-Reed, and Smita S. Patel. "Structure, mechanism, and regulation of mitochondrial DNA transcription initiation." Journal of Biological Chemistry 295, no. 52 (October 30, 2020): 18406–25. http://dx.doi.org/10.1074/jbc.rev120.011202.

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Mitochondria are specialized compartments that produce requisite ATP to fuel cellular functions and serve as centers of metabolite processing, cellular signaling, and apoptosis. To accomplish these roles, mitochondria rely on the genetic information in their small genome (mitochondrial DNA) and the nucleus. A growing appreciation for mitochondria's role in a myriad of human diseases, including inherited genetic disorders, degenerative diseases, inflammation, and cancer, has fueled the study of biochemical mechanisms that control mitochondrial function. The mitochondrial transcriptional machinery is different from nuclear machinery. The in vitro re-constituted transcriptional complexes of Saccharomyces cerevisiae (yeast) and humans, aided with high-resolution structures and biochemical characterizations, have provided a deeper understanding of the mechanism and regulation of mitochondrial DNA transcription. In this review, we will discuss recent advances in the structure and mechanism of mitochondrial transcription initiation. We will follow up with recent discoveries and formative findings regarding the regulatory events that control mitochondrial DNA transcription, focusing on those involved in cross-talk between the mitochondria and nucleus.

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Piruat, José I., Sebastián Chávez, and Andrés Aguilera. "The Yeast HRS1 Gene Is Involved in Positive and Negative Regulation of Transcription and Shows Genetic Characteristics Similar to SIN4 and GAL11." Genetics 147, no. 4 (December 1, 1997): 1585–94. http://dx.doi.org/10.1093/genetics/147.4.1585.

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Abstract We provide genetic evidence that HRS1/PGD1, a yeast gene previously identified as a suppressor of the hyper-recombination phenotype of hpr1, has positive and negative roles in transcriptional regulation. We have analyzed three differently regulated promoters, GAL1, PHO5 and HSP26, by β-galactosidase assays of lacZ-fused promoters and by Northern analysis of the endogenous genes. Transcription of these promoters was derepressed in hrs1Δ mutants under conditions in which it is normally repressed in wild type, Under induced conditions it was either strongly reduced or significantly enhanced depending on the promoter system analyzed. Constitutive transcription was not affected, as determined in ADH1 and TEF2. In addition, Hrs1p was required for mating-factor expression, telomere-linked DNA silencing and DNA supercoiling of plasmids. Furthermore, hrs1Δ suppressed Ty-insertion mutations and conferred a Gal−-phenotype. Many of these phenotypes also result from mutations in GAL11, SIN4 or RGR1, which encode proteins of the RNA polII mediator. We also show that gal11Δ and sin4Δ partially suppress the hyper-rec phenotype of hpr1 mutants, although to a lesser extent than hrs1Δ. Our results provide new evidence for the connection between hrs1Δ-induced deletions and transcription. We discuss the possibility that Hrs1p might be a component of the RNA polII transcription machinery.

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van Ouwerkerk, Antoinette F., Amelia W. Hall, Zachary A. Kadow, Sonja Lazarevic, Jasmeet S. Reyat, Nathan R. Tucker, Rangarajan D. Nadadur, et al. "Epigenetic and Transcriptional Networks Underlying Atrial Fibrillation." Circulation Research 127, no. 1 (June 19, 2020): 34–50. http://dx.doi.org/10.1161/circresaha.120.316574.

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Genome-wide association studies have uncovered over a 100 genetic loci associated with atrial fibrillation (AF), the most common arrhythmia. Many of the top AF-associated loci harbor key cardiac transcription factors, including PITX2, TBX5, PRRX1, and ZFHX3. Moreover, the vast majority of the AF-associated variants lie within noncoding regions of the genome where causal variants affect gene expression by altering the activity of transcription factors and the epigenetic state of chromatin. In this review, we discuss a transcriptional regulatory network model for AF defined by effector genes in Genome-wide association studies loci. We describe the current state of the field regarding the identification and function of AF-relevant gene regulatory networks, including variant regulatory elements, dose-sensitive transcription factor functionality, target genes, and epigenetic states. We illustrate how altered transcriptional networks may impact cardiomyocyte function and ionic currents that impact AF risk. Last, we identify the need for improved tools to identify and functionally test transcriptional components to define the links between genetic variation, epigenetic gene regulation, and atrial function.

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Datar, Ila, Hanna Tegegne, Kevin Qin, Fahd Al-Mulla, Milad S. Bitar, Robert J. Trumbly, and Kam C. Yeung. "Genetic and Epigenetic Control of RKIP Transcription." Critical Reviews in Oncogenesis 19, no. 6 (2014): 417–30. http://dx.doi.org/10.1615/critrevoncog.2014012025.

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Mochdia, Keiichi, and Shun Tamaki. "Transcription Factor-Based Genetic Engineering in Microalgae." Plants 10, no. 8 (August 4, 2021): 1602. http://dx.doi.org/10.3390/plants10081602.

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Sequence-specific DNA-binding transcription factors (TFs) are key components of gene regulatory networks. Advances in high-throughput sequencing have facilitated the rapid acquisition of whole genome assembly and TF repertoires in microalgal species. In this review, we summarize recent advances in gene discovery and functional analyses, especially for transcription factors in microalgal species. Specifically, we provide examples of the genome-scale identification of transcription factors in genome-sequenced microalgal species and showcase their application in the discovery of regulators involved in various cellular functions. Herein, we highlight TF-based genetic engineering as a promising framework for designing microalgal strains for microalgal-based bioproduction.

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Wierda, Rutger, and Peter van den Elsen. "Genetic and Epigenetic Regulation of CCR5 Transcription." Biology 1, no. 3 (December 13, 2012): 869–79. http://dx.doi.org/10.3390/biology1030869.

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Kim, Kwoneel, Hyoeun Bang, Kibaick Lee, and Jung Kyoon Choi. "Genetic Architecture of Transcription and Chromatin Regulation." Genomics & Informatics 13, no. 2 (2015): 40. http://dx.doi.org/10.5808/gi.2015.13.2.40.

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Kafri, Ran, Arren Bar-Even, and Yitzhak Pilpel. "Transcription control reprogramming in genetic backup circuits." Nature Genetics 37, no. 3 (February 20, 2005): 295–99. http://dx.doi.org/10.1038/ng1523.

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COTSAPAS, C., E. CHAN, M. KIRK, M. TANAKA, and P. LITTLE. "Genetic Variation and the Control of Transcription." Cold Spring Harbor Symposia on Quantitative Biology 68 (January 1, 2003): 109–14. http://dx.doi.org/10.1101/sqb.2003.68.109.

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Weber, W., S. Luzi, M. Karlsson, C. D. Sanchez-Bustamante, U. Frey, A. Hierlemann, and M. Fussenegger. "A synthetic mammalian electro-genetic transcription circuit." Nucleic Acids Research 37, no. 4 (December 18, 2008): e33-e33. http://dx.doi.org/10.1093/nar/gkp014.

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Edelman, Lucas Brandon, and Peter Fraser. "Transcription factories: genetic programming in three dimensions." Current Opinion in Genetics & Development 22, no. 2 (April 2012): 110–14. http://dx.doi.org/10.1016/j.gde.2012.01.010.

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Keller, Andrew D. "Model genetic circuits encoding autoregulatory transcription factors." Journal of Theoretical Biology 172, no. 2 (January 1995): 169–85. http://dx.doi.org/10.1006/jtbi.1995.0014.

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Santpere, Gabriel. "Genetic Variation in Transcription Factor Binding Sites." International Journal of Molecular Sciences 24, no. 5 (March 6, 2023): 5038. http://dx.doi.org/10.3390/ijms24055038.

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Lauder, S., M. Bankmann, S. N. Guzder, P. Sung, L. Prakash, and S. Prakash. "Dual requirement for the yeast MMS19 gene in DNA repair and RNA polymerase II transcription." Molecular and Cellular Biology 16, no. 12 (December 1996): 6783–93. http://dx.doi.org/10.1128/mcb.16.12.6783.

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Genetic and biochemical studies of Saccharomyces cerevisiae have indicated the involvement of a large number of protein factors in nucleotide excision repair (NER) of UV-damaged DNA. However, how MMS19 affects this process has remained unclear. Here, we report on the isolation of the MMS19 gene and the determination of its role in NER and other cellular processes. Genetic and biochemical evidence indicates that besides its function in NER, MMS19 also affects RNA polymerase II (Pol II) transcription. mms19delta cells do not grow at 37 degrees C, and mutant extract exhibits a thermolabile defect in Pol II transcription. Thus, Mms19 protein resembles TFIIH in that it is required for both transcription and DNA repair. However, addition of purified Mms19 protein does not alleviate the transcriptional defect of the mms19delta extract, nor does it stimulate the incision of UV-damaged DNA reconstituted from purified proteins. Interestingly, addition of purified TFIIH corrects the transcriptional defect of the mms19delta extract. Mms19 is, however, not a component of TFIIH or of Pol II holoenzyme. These and other results suggest that Mms19 affects NER and transcription by influencing the activity of TFIIH as an upstream regulatory element. It is proposed that mutations in the human MMS19 counterpart could result in syndromes in which both NER and transcription are affected.

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Swanson, M. S., and F. Winston. "SPT4, SPT5 and SPT6 interactions: effects on transcription and viability in Saccharomyces cerevisiae." Genetics 132, no. 2 (October 1, 1992): 325–36. http://dx.doi.org/10.1093/genetics/132.2.325.

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Abstract The SPT4, SPT5 and SPT6 genes of Saccharomyces cerevisiae were identified originally by mutations that suppress delta insertion mutations at HIS4 and LYS2. Subsequent analysis has demonstrated that spt4, spt5 and spt6 mutations confer similar pleiotropic phenotypes. They suppress delta insertion mutations by altering transcription and are believed to be required for normal transcription of several other loci. We have now analyzed interactions between SPT4, SPT5 and SPT6. First, the combination of mutations in any two of these three genes causes lethality in haploids. Second, some recessive mutations in different members of this set fail to complement each other. Third, mutations in all three genes alter transcription in similar ways. Finally, the results of coimmunoprecipitation experiments demonstrate that at least the SPT5 and SPT6 proteins interact physically. Taken together, these genetic and biochemical results indicate that SPT4, SPT5 and SPT6 function together in a transcriptional process that is essential for viability in yeast.

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Ignatieva, E. V., and E. A. Matrosova. "Disease-associated genetic variants in the regulatory regions of human genes: mechanisms of action on transcription and genomic resources for dissecting these mechanisms." Vavilov Journal of Genetics and Breeding 25, no. 1 (March 16, 2021): 18–29. http://dx.doi.org/10.18699/vj21.003.

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Whole genome and whole exome sequencing technologies play a very important role in the studies of the genetic aspects of the pathogenesis of various diseases. The ample use of genome-wide and exome-wide association study methodology (GWAS and EWAS) made it possible to identify a large number of genetic variants associated with diseases. This information is accumulated in the databases like GWAS central, GWAS catalog, OMIM, ClinVar, etc. Most of the variants identified by the GWAS technique are located in the noncoding regions of the human genome. According to the ENCODE project, the fraction of regions in the human genome potentially involved in transcriptional control is many times greater than the fraction of coding regions. Thus, genetic variation in noncoding regions of the genome can increase the susceptibility to diseases by disrupting various regulatory elements (promoters, enhancers, silencers, insulator regions, etc.). However, identification of the mechanisms of influence of pathogenic genetic variants on the diseases risk is difficult due to a wide variety of regulatory elements. The present review focuses on the molecular genetic mechanisms by which pathogenic genetic variants affect gene expression. At the same time, attention is concentrated on the transcriptional level of regulation as an initial step in the expression of any gene. A triggering event mediating the effect of a pathogenic genetic variant on the level of gene expression can be, for example, a change in the functional activity of transcription factor binding sites (TFBSs) or DNA methylation change, which, in turn, affects the functional activity of promoters or enhancers. Dissecting the regulatory roles of polymorphic loci have been impossible without close integration of modern experimental approaches with computer analysis of a growing wealth of genetic and biological data obtained using omics technologies. The review provides a brief description of a number of the most well-known public genomic information resources containing data obtained using omics technologies, including (1) resources that accumulate data on the chromatin states and the regions of transcription factor binding derived from ChIP-seq experiments; (2) resources containing data on genomic loci, for which allele-specific transcription factor binding was revealed based on ChIP-seq technology; (3) resources containing in silico predicted data on the potential impact of genetic variants on the transcription factor binding sites.

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Scholz, H., J. Deatrick, A. Klaes, and C. Klämbt. "Genetic dissection of pointed, a Drosophila gene encoding two ETS-related proteins." Genetics 135, no. 2 (October 1, 1993): 455–68. http://dx.doi.org/10.1093/genetics/135.2.455.

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Abstract The Drosophila gene pointed (pnt) is required for the differentiation of a number of tissues during embryogenesis, including the ventral ectoderm, the nervous system, the tracheal system and certain muscle fibers. The phenotypes associated with strong pointed alleles are reflected by a complex pointed expression pattern during embryogenesis. Two promoters, P1 and P2, separated by some 50 kb of genomic sequences, direct the transcription of two different transcript forms, encoding two different proteins related to the ETS family of transcription factors. To assess the individual functions of the two different pointed protein forms, we have generated new pointed alleles affecting either the P1 or the P2 transcript, termed P1 and P2 alleles, respectively. Genetic analysis reveals partial heteroallelic complementation between certain pointed P1 and P2 alleles. Surviving trans-heterozygous flies have rough eyes, abnormal wings and halters, suggesting a requirement for pointed function during their imaginal disc development. Further genetic analysis demonstrates that expression of a given pointed P2 allele depends on trans-acting transcriptional regulatory sequences. We have identified two chromosomal domains with opposite regulatory effects on the transcriptional activity of the pointed P2 promoter, one trans-activates and the other trans-represses pointed P2 expression. By deletion mapping we were able to localize these control regions within the 5' region of the pointed P2 transcript.

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Augustin, Regina, Stefan F. Lichtenthaler, Michael Greeff, Jens Hansen, Wolfgang Wurst, and Dietrich Trümbach. "Bioinformatics Identification of Modules of Transcription Factor Binding Sites in Alzheimer's Disease-Related Genes by In Silico Promoter Analysis and Microarrays." International Journal of Alzheimer's Disease 2011 (2011): 1–13. http://dx.doi.org/10.4061/2011/154325.

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The molecular mechanisms and genetic risk factors underlying Alzheimer's disease (AD) pathogenesis are only partly understood. To identify new factors, which may contribute to AD, different approaches are taken including proteomics, genetics, and functional genomics. Here, we used a bioinformatics approach and found that distinct AD-related genes share modules of transcription factor binding sites, suggesting a transcriptional coregulation. To detect additional coregulated genes, which may potentially contribute to AD, we established a new bioinformatics workflow with known multivariate methods like support vector machines, biclustering, and predicted transcription factor binding site modules by using in silico analysis and over 400 expression arrays from human and mouse. Two significant modules are composed of three transcription factor families: CTCF, SP1F, and EGRF/ZBPF, which are conserved between human and mouse APP promoter sequences. The specific combination of in silico promoter and multivariate analysis can identify regulation mechanisms of genes involved in multifactorial diseases.

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Muller, Ryan, Zuriah A. Meacham, Lucas Ferguson, and Nicholas T. Ingolia. "CiBER-seq dissects genetic networks by quantitative CRISPRi profiling of expression phenotypes." Science 370, no. 6522 (December 10, 2020): eabb9662. http://dx.doi.org/10.1126/science.abb9662.

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To realize the promise of CRISPR-Cas9–based genetics, approaches are needed to quantify a specific, molecular phenotype across genome-wide libraries of genetic perturbations. We addressed this challenge by profiling transcriptional, translational, and posttranslational reporters using CRISPR interference (CRISPRi) with barcoded expression reporter sequencing (CiBER-seq). Our barcoding approach allowed us to connect an entire library of guides to their individual phenotypic consequences using pooled sequencing. CiBER-seq profiling fully recapitulated the integrated stress response (ISR) pathway in yeast. Genetic perturbations causing uncharged transfer RNA (tRNA) accumulation activated ISR reporter transcription. Notably, tRNA insufficiency also activated the reporter, independent of the uncharged tRNA sensor. By uncovering alternate triggers for ISR activation, we illustrate how precise, comprehensive CiBER-seq profiling provides a powerful and broadly applicable tool for dissecting genetic networks.

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Martinez-Argudo, I., R. Little, N. Shearer, P. Johnson, and R. Dixon. "Nitrogen fixation: key genetic regulatory mechanisms." Biochemical Society Transactions 33, no. 1 (February 1, 2005): 152–56. http://dx.doi.org/10.1042/bst0330152.

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The necessity to respond to the level of fixed nitrogen and external oxygen concentrations and to provide sufficient energy for nitrogen fixation imposes common regulatory principles amongst diazotrophs. The NifL–NifA system in Azotobacter vinelandii integrates the signals of redox, fixed-nitrogen and carbon status to regulate nif transcription. Multidomain signalling interactions between NifL and NifA are modulated by redox changes, ligand binding and interaction with the signal-transduction protein GlnK. Under adverse redox conditions (excess oxygen) or when fixed nitrogen is in excess, NifL forms a complex with NifA in which transcriptional activation is prevented. Oxidized NifL forms a binary complex with NifA to inhibit NifA activity. When fixed nitrogen is in excess, the non-covalently modified form of GlnK interacts with NifL to promote the formation of a GlnK–NifL–NifA ternary complex. When the cell re-encounters favourable conditions for nitrogen fixation, it is necessary to deactivate the signals to ensure that the NifL–NifA complex is dissociated so that NifA is free to activate transcription. This is achieved through interactions with 2-oxoglutarate, a key metabolic signal of the carbon status, which binds to the N-terminal GAF (cGMP-specific and stimulated phosphodiesterases, Anabaena adenylate cyclases and Escherichia coliFhlA) domain of NifA.

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Ellison, Mitchell A., Alex R. Lederer, Marcie H. Warner, Travis N. Mavrich, Elizabeth A. Raupach, Lawrence E. Heisler, Corey Nislow, Miler T. Lee, and Karen M. Arndt. "The Paf1 Complex Broadly Impacts the Transcriptome of Saccharomyces cerevisiae." Genetics 212, no. 3 (May 15, 2019): 711–28. http://dx.doi.org/10.1534/genetics.119.302262.

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The Polymerase Associated Factor 1 complex (Paf1C) is a multifunctional regulator of eukaryotic gene expression important for the coordination of transcription with chromatin modification and post-transcriptional processes. In this study, we investigated the extent to which the functions of Paf1C combine to regulate the Saccharomyces cerevisiae transcriptome. While previous studies focused on the roles of Paf1C in controlling mRNA levels, here, we took advantage of a genetic background that enriches for unstable transcripts, and demonstrate that deletion of PAF1 affects all classes of Pol II transcripts including multiple classes of noncoding RNAs (ncRNAs). By conducting a de novo differential expression analysis independent of gene annotations, we found that Paf1 positively and negatively regulates antisense transcription at multiple loci. Comparisons with nascent transcript data revealed that many, but not all, changes in RNA levels detected by our analysis are due to changes in transcription instead of post-transcriptional events. To investigate the mechanisms by which Paf1 regulates protein-coding genes, we focused on genes involved in iron and phosphate homeostasis, which were differentially affected by PAF1 deletion. Our results indicate that Paf1 stimulates phosphate gene expression through a mechanism that is independent of any individual Paf1C-dependent histone modification. In contrast, the inhibition of iron gene expression by Paf1 correlates with a defect in H3 K36 trimethylation. Finally, we showed that one iron regulon gene, FET4, is coordinately controlled by Paf1 and transcription of upstream noncoding DNA. Together, these data identify roles for Paf1C in controlling both coding and noncoding regions of the yeast genome.

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Kędzierska-Mieszkowska, Sabina, Katarzyna Potrykus, Zbigniew Arent, and Joanna Krajewska. "Identification of σE-Dependent Promoter Upstream of clpB from the Pathogenic Spirochaete Leptospira interrogans by Applying an E. coli Two-Plasmid System." International Journal of Molecular Sciences 20, no. 24 (December 15, 2019): 6325. http://dx.doi.org/10.3390/ijms20246325.

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There is limited information on gene expression in the pathogenic spirochaete Leptospira interrogans and genetic mechanisms controlling its virulence. Transcription is the first step in gene expression that is often determined by environmental effects, including infection-induced stresses. Alterations in the environment result in significant changes in the transcription of many genes, allowing effective adaptation of Leptospira to mammalian hosts. Thus, promoter and transcriptional start site identification are crucial for determining gene expression regulation and for the understanding of genetic regulatory mechanisms existing in Leptospira. Here, we characterized the promoter region of the L. interrogans clpB gene (clpBLi) encoding an AAA+ molecular chaperone ClpB essential for the survival of this spirochaete under thermal and oxidative stresses, and also during infection of the host. Primer extension analysis demonstrated that transcription of clpB in L. interrogans initiates at a cytidine located 41 bp upstream of the ATG initiation codon, and, to a lesser extent, at an adenine located 2 bp downstream of the identified site. Transcription of both transcripts was heat-inducible. Determination of clpBLi transcription start site, combined with promoter transcriptional activity assays using a modified two-plasmid system in E. coli, revealed that clpBLi transcription is controlled by the ECF σE factor. Of the ten L. interrogans ECF σ factors, the factor encoded by LIC_12757 (LA0876) is most likely to be the key regulator of clpB gene expression in Leptospira cells, especially under thermal stress. Furthermore, clpB expression may be mediated by ppGpp in Leptospira.

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Freedman, Jennifer A., and Sue Jinks-Robertson. "Genetic Requirements for Spontaneous and Transcription-Stimulated Mitotic Recombination inSaccharomyces cerevisiae." Genetics 162, no. 1 (September 1, 2002): 15–27. http://dx.doi.org/10.1093/genetics/162.1.15.

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AbstractThe genetic requirements for spontaneous and transcription-stimulated mitotic recombination were determined using a recombination system that employs heterochromosomal lys2 substrates that can recombine only by crossover or only by gene conversion. The substrates were fused either to a constitutive low-level promoter (pLYS) or to a highly inducible promoter (pGAL). In the case of the “conversion-only” substrates the use of heterologous promoters allowed either the donor or the recipient allele to be highly transcribed. Transcription of the donor allele stimulated gene conversions in rad50, rad51, rad54, and rad59 mutants, but not in rad52, rad55, and rad57 mutants. In contrast, transcription of the recipient allele stimulated gene conversions in rad50, rad51, rad54, rad55, rad57, and rad59 mutants, but not in rad52 mutants. Finally, transcription stimulated crossovers in rad50, rad54, and rad59 mutants, but not in rad51, rad52, rad55, and rad57 mutants. These data are considered in relation to previously proposed molecular mechanisms of transcription-stimulated recombination and in relation to the roles of the recombination proteins.

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Cox, James Shell, and Michael W. Van Dyke. "General and Genomic DNA-Binding Specificity for the Thermus thermophilus HB8 Transcription Factor TTHB023." Biomolecules 10, no. 1 (January 6, 2020): 94. http://dx.doi.org/10.3390/biom10010094.

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Transcription factors are proteins that recognize specific DNA sequences and affect local transcriptional processes. They are the primary means by which all organisms control specific gene expression. Understanding which DNA sequences a particular transcription factor recognizes provides important clues into the set of genes that they regulate and, through this, their potential biological functions. Insights may be gained through homology searches and genetic means. However, these approaches can be misleading, especially when comparing distantly related organisms or in cases of complicated transcriptional regulation. In this work, we used a biochemistry-based approach to determine the spectrum of DNA sequences specifically bound by the Thermus thermophilus HB8 TetR-family transcription factor TTHB023. The consensus sequence 5′–(a/c)Y(g/t)A(A/C)YGryCR(g/t)T(c/a)R(g/t)–3′ was found to have a nanomolar binding affinity with TTHB023. Analyzing the T. thermophilus HB8 genome, several TTHB023 consensus binding sites were mapped to the promoters of genes involved in fatty acid biosynthesis. Notably, some of these were not identified previously through genetic approaches, ostensibly given their potential co-regulation by the Thermus thermophilus HB8 TetR-family transcriptional repressor TTHA0167. Our investigation provides additional evidence supporting the usefulness of a biochemistry-based approach for characterizing putative transcription factors, especially in the case of cooperative regulation.

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Sommer, Hans, Wolfgang Nacken, Pio Beltran, Peter Huijser, Heike Pape, Rolf Hansen, Peter Flor, Heinz Saedler, and Zsuzsanna Schwarz-Sommer. "Properties of deficiens, a homeotic gene involved in the control of flower morphogenesis in Antirrhinum majus." Development 113, Supplement_1 (January 1, 1991): 169–75. http://dx.doi.org/10.1242/dev.113.supplement_1.169.

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deficiens, together with other homeotic genes, is involved in the genetic control of floral morphogenesis in A. majus. Mutations in this gene cause homeotic transformations of petals to sepals and stamens to carpels, thus producing male sterile flowers. The deduced DEF A protein shows homology to the DNA-binding domain of the transcription factors SRF of mammals (activating c-fos) and MCM1 of yeast (regulating mating type), suggesting that DEF A has a possible regulatory function as a transcription factor. Interestingly, DEF A belongs to a family of putative transcription factors, called the MADS box genes, whose DNA-binding domains show conserved homology. Two members of this family correlate with known morphogenetic mutants of Antirrhinum. DEF A is constantly expressed during flower development in all floral organs; it is strongly expressed in petals and stamens, but only at a low basal level in the other organs. Molecular, genetic and morphological observations with deficiens morphoalleles indicate that transcriptional and post-transcriptional control of deficiens specifies and diversifies its function in space and time.

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Poulat, Francis. "Non-Coding Genome, Transcription Factors, and Sex Determination." Sexual Development 15, no. 5-6 (2021): 295–307. http://dx.doi.org/10.1159/000519725.

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In vertebrates, gonadal sex determination is the process by which transcription factors drive the choice between the testicular and ovarian identity of undifferentiated somatic progenitors through activation of 2 different transcriptional programs. Studies in animal models suggest that sex determination always involves sex-specific transcription factors that activate or repress sex-specific genes. These transcription factors control their target genes by recognizing their regulatory elements in the non-coding genome and their binding motifs within their DNA sequence. In the last 20 years, the development of genomic approaches that allow identifying all the genomic targets of a transcription factor in eukaryotic cells gave the opportunity to globally understand the function of the nuclear proteins that control complex genetic programs. Here, the major transcription factors involved in male and female vertebrate sex determination and the genomic profiling data of mouse gonads that contributed to deciphering their transcriptional regulation role will be reviewed.

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Gallardo, Mercedes, and Andrés Aguilera. "A New Hyperrecombination Mutation Identifies a Novel Yeast Gene, THP1, Connecting Transcription Elongation With Mitotic Recombination." Genetics 157, no. 1 (January 1, 2001): 79–89. http://dx.doi.org/10.1093/genetics/157.1.79.

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Abstract Given the importance of the incidence of recombination in genomic instability, it is of great interest to know the elements or processes controlling recombination in mitosis. One such process is transcription, which has been shown to induce recombination in bacteria, yeast, and mammals. To further investigate the genetic control of the incidence of recombination and genetic instability and, in particular, its connection with transcription, we have undertaken a search for hyperrecombination mutants among a large number of strains deleted in genes of unknown function. We have identified a new gene, THP1 (YOL072w), whose deletion mutation strongly stimulates recombination between repeats. In addition, thp1Δ impairs transcription, a defect that is particularly strong at the level of elongation through particular DNA sequences such as lacZ. The hyperrecombination phenotype of thp1Δ cells is fully dependent on transcription elongation of the repeat construct. When transcription is impeded either by shutting off the promoter or by using a premature transcription terminator, hyperrecombination between repeats is abolished, providing new evidence that transcription-elongation impairment may be a source of recombinogenic substrates in mitosis. We show that Thp1p and two other proteins previously shown to control transcription-associated recombination, Hpr1p and Tho2p, act in the same “pathway” connecting transcription elongation with the incidence of mitotic recombination.

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Aliotta, Jason M., Mandy Pereira, Mark Dooner, Gerri Dooner, Bharat Ramratnam, David Lee, Kevin Johnson, et al. "Microvesicle Mediated Genetic Phenotype Modulation." Blood 114, no. 22 (November 20, 2009): 4509. http://dx.doi.org/10.1182/blood.v114.22.4509.4509.

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Abstract Abstract 4509 Objective We have previously reported that lung-derived microvesicles (MVs) can enter target marrow cells, resulting in increased levels of lung-specific mRNAs (Stem Cells 25:2245, 2007). Marrow cells which have been exposed to MVs also show increased production of pulmonary epithelial cells after transplantation into irradiated mice. The present studies have addressed the universality of the mRNA modulation and the underlying mechanisms. Methods/Results Co-culture of heart, brain, liver, and lung tissue across from murine marrow, but separated by a 0.4 micron cell-impermeable membrane, show tissue specific elevations of mRNA. MVs were found to contain lung-specific mRNA and 200 microRNAs. Proteomic studies of MVs showed up to 75 individual proteins, some of which are known to be associated with MV biogenesis and trafficking. Studies using rat/mouse hybrid cultures demonstrated that the target cell induced lung-specific mRNA elevations were mediated by transcriptional mechanisms. In these experiments, rat lung was co-cultured across from murine marrow cells and RT-PCR was performed using rat or mouse-specific primers for surfactant B. High levels of rat-specific surfactant B were seen in the co-cultured marrow cells indicating that transcription had been induced in the target cells. These conclusions were supported by additional studies employing the transcription factor inhibitors actinomycin-D and alpha-amantin. RNase treatment of conditioned media prior to marrow cell co-culture suggested that transfer of RNA may be involved in these mRNA elevations. However, our transcriptional studies indicate that we are not observing a simple transfer of MV lung-specific mRNA. One possible mechanism may be transfer of microRNA with epigenetic changes resulting in lung-specific mRNA production. Conclusion In summary, these observations suggest the existence of unique pathways for information transfer and cell phenotype determination. MV transfer could represent an underlying mechanism for much of the previous reported stem cell plasticity in different tissues. Disclosures: No relevant conflicts of interest to declare.

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Hayashi, Shunya, Mutsumi Watanabe, Makoto Kobayashi, Takayuki Tohge, Takashi Hashimoto, and Tsubasa Shoji. "Genetic Manipulation of Transcriptional Regulators Alters Nicotine Biosynthesis in Tobacco." Plant and Cell Physiology 61, no. 6 (March 19, 2020): 1041–53. http://dx.doi.org/10.1093/pcp/pcaa036.

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Abstract The toxic alkaloid nicotine is produced in the roots of Nicotiana species and primarily accumulates in leaves as a specialized metabolite. A series of metabolic and transport genes involved in the nicotine pathway are coordinately upregulated by a pair of jasmonate-responsive AP2/ERF-family transcription factors, NtERF189 and NtERF199, in the roots of Nicotiana tabacum (tobacco). In this study, we explored the potential of manipulating the expression of these transcriptional regulators to alter nicotine biosynthesis in tobacco. The transient overexpression of NtERF189 led to alkaloid production in the leaves of Nicotiana benthamiana and Nicotiana alata. This ectopic production was further enhanced by co-overexpressing a gene encoding a basic helix-loop-helix-family MYC2 transcription factor. Constitutive and leaf-specific overexpression of NtERF189 increased the accumulation of foliar alkaloids in transgenic tobacco plants but negatively affected plant growth. By contrast, in a knockout mutant of NtERF189 and NtERF199 obtained through CRISPR/Cas9-based genome editing, alkaloid levels were drastically reduced without causing major growth defects. Metabolite profiling revealed the impact of manipulating the nicotine pathway on a wide range of nitrogen- and carbon-containing metabolites. Our findings provide insights into the biotechnological applications of engineering metabolic pathways by targeting transcription factors.

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Journal articles on the topic 'Genetic transcription'

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