Journal articles on the topic 'Rho-dependent termination'

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1

Ciampi, M. Sofia. "Rho-dependent terminators and transcription termination." Microbiology 152, no. 9 (September 1, 2006): 2515–28. http://dx.doi.org/10.1099/mic.0.28982-0.

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Rho-dependent transcription terminators participate in sophisticated genetic regulatory mechanisms, in both bacteria and phages; they occur in regulatory regions preceding the coding sequences of genes and within coding sequences, as well as at the end of transcriptional units, to prevent readthrough transcription. Most Rho-dependent terminators have been found in enteric bacteria, but they also occur in Gram-positive bacteria and may be widespread among bacteria. Rho-dependent termination requires both cis-acting elements, on the mRNA, and trans-acting factors. The only cis-acting element common to Rho-dependent terminators is richness in rC residues. Additional sequence elements have been observed at different Rho termination sites. These ‘auxiliary elements' may assist in the termination process; they differ among terminators, their occurrence possibly depending on the function and sequence context of the terminator. Specific nucleotides required for termination have also been identified at Rho sites. Rho is the main factor required for termination; it is a ring-shaped hexameric protein with ATPase and helicase activities. NusG, NusA and NusB are additional factors participating in the termination process. Rho-dependent termination occurs by binding of Rho to ribosome-free mRNA, C-rich sites being good candidates for binding. Rho's ATPase is activated by Rho–mRNA binding, and provides the energy for Rho translocation along the mRNA; translocation requires sliding of the message into the central hole of the hexamer. When a polymerase pause site is encountered, the actual termination occurs, and the transcript is released by Rho's helicase activity. Many aspects of this process are still being studied. The isolation of mutants suppressing termination, site-directed mutagenesis of cis-acting elements in Rho-dependent termination, and biochemistry, are and will be contributing to unravelling the still undefined aspects of the Rho termination machinery. Analysis of the more sophisticated regulatory mechanisms relying on Rho-dependent termination may be crucial in identifying new essential elements for termination.
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2

Richardson, John P. "Rho-dependent transcription termination." Biochimica et Biophysica Acta (BBA) - Gene Structure and Expression 1048, no. 2-3 (April 1990): 127–38. http://dx.doi.org/10.1016/0167-4781(90)90048-7.

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3

Richardson, John P., and E. Cristy Ruteshouser. "rho Factor-dependent transcription termination." Journal of Molecular Biology 189, no. 3 (June 1986): 413–19. http://dx.doi.org/10.1016/0022-2836(86)90313-x.

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4

Richardson, John P. "Rho-dependent termination and ATPases in transcript termination." Biochimica et Biophysica Acta (BBA) - Gene Structure and Expression 1577, no. 2 (September 2002): 251–60. http://dx.doi.org/10.1016/s0167-4781(02)00456-6.

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5

Hinde, Paul, Padraig Deighan, and Charles J. Dorman. "Characterization of the Detachable Rho-Dependent Transcription Terminator of the fimE Gene in Escherichia coli K-12." Journal of Bacteriology 187, no. 24 (December 15, 2005): 8256–66. http://dx.doi.org/10.1128/jb.187.24.8256-8266.2005.

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ABSTRACT The fim genetic switch in the chromosome of Escherichia coli K-12 is an invertible DNA element that harbors the promoter for transcription of the downstream fim structural genes and a transcription terminator that acts on the upstream fimE regulatory gene. Switches oriented appropriately for structural gene transcription also allow fimE mRNA to read through, whereas those in the opposite orientation terminate the fimE message. We show here that termination is Rho dependent and is suppressed in a rho mutant or by bicyclomycin treatment when fimE mRNA is expressed by the fimE gene, either from a multicopy recombinant plasmid or in its native chromosomal location. Two cis-acting elements within the central portion of the 314-bp invertible DNA switch were identified as contributors to Rho-dependent termination and dissected. These fim sequence elements show similarities to well-characterized Rho utilization (rut) sites and consist of a boxA motif and a C-rich and G-poor region of approximately 40 bp. Deletion of the boxA motif alone had only a subtle negative effect on Rho function. However, when this element was deleted in combination with the C-rich, G-poor region, Rho function was considerably decreased. Altering the C-to-G ratio in favor of G in this portion of the switch also strongly attenuated transcription termination. The implications of the existence of a fimE-specific Rho-dependent terminator within the invertible switch are discussed in the context of the fim regulatory circuit.
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6

Hao, Zhitai, Vladimir Svetlov, and Evgeny Nudler. "Rho-dependent transcription termination: a revisionist view." Transcription 12, no. 4 (August 8, 2021): 171–81. http://dx.doi.org/10.1080/21541264.2021.1991773.

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7

Hollands, K., S. Proshkin, S. Sklyarova, V. Epshtein, A. Mironov, E. Nudler, and E. A. Groisman. "Riboswitch control of Rho-dependent transcription termination." Proceedings of the National Academy of Sciences 109, no. 14 (March 19, 2012): 5376–81. http://dx.doi.org/10.1073/pnas.1112211109.

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8

Sevostyanova, Anastasia, and Eduardo A. Groisman. "An RNA motif advances transcription by preventing Rho-dependent termination." Proceedings of the National Academy of Sciences 112, no. 50 (November 16, 2015): E6835—E6843. http://dx.doi.org/10.1073/pnas.1515383112.

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The transcription termination factor Rho associates with most nascent bacterial RNAs as they emerge from RNA polymerase. However, pharmacological inhibition of Rho derepresses only a small fraction of these transcripts. What, then, determines the specificity of Rho-dependent transcription termination? We now report the identification of a Rho-antagonizing RNA element (RARE) that hinders Rho-dependent transcription termination. We establish that RARE traps Rho in an inactive complex but does not prevent Rho binding to its recruitment sites. Although translating ribosomes normally block Rho access to an mRNA, inefficient translation of an open reading frame in the leader region of the Salmonella mgtCBR operon actually enables transcription of its associated coding region by favoring an RNA conformation that sequesters RARE. The discovery of an RNA element that inactivates Rho signifies that the specificity of nucleic-acid binding proteins is defined not only by the sequences that recruit these proteins but also by sequences that antagonize their activity.
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9

Zhu, Anne Q., and Peter H. von Hippel. "Rho-dependent Termination within thetrp t‘ Terminator. I. Effects of Rho Loading and Template Sequence†." Biochemistry 37, no. 32 (August 1998): 11202–14. http://dx.doi.org/10.1021/bi9729110.

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10

Zhu, Anne Q., and Peter H. von Hippel. "Rho-dependent Termination within thetrp t ‘ Terminator. II. Effects of Kinetic Competition and Rho Processivity†." Biochemistry 37, no. 32 (August 1998): 11215–22. http://dx.doi.org/10.1021/bi972912s.

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11

Silva, Inês Jesus, Susana Barahona, Alex Eyraud, David Lalaouna, Nara Figueroa-Bossi, Eric Massé, and Cecília Maria Arraiano. "SraL sRNA interaction regulates the terminator by preventing premature transcription termination of rho mRNA." Proceedings of the National Academy of Sciences 116, no. 8 (February 4, 2019): 3042–51. http://dx.doi.org/10.1073/pnas.1811589116.

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Transcription termination is a critical step in the control of gene expression. One of the major termination mechanisms is mediated by Rho factor that dissociates the complex mRNA-DNA-RNA polymerase upon binding with RNA polymerase. Rho promotes termination at the end of operons, but it can also terminate transcription within leader regions, performing regulatory functions and avoiding pervasive transcription. Transcription of rho is autoregulated through a Rho-dependent attenuation in the leader region of the transcript. In this study, we have included an additional player in this pathway. By performing MS2-affinity purification coupled with RNA sequencing (MAPS), rho transcript was shown to directly interact with the small noncoding RNA SraL. Using bioinformatic in vivo and in vitro experimental analyses, SraL was shown to base pair with the 5′-UTR of rho mRNA upregulating its expression in several growth conditions. This base pairing was shown to prevent the action of Rho over its own message. Moreover, the results obtained indicate that both ProQ and Hfq are associated with this regulation. We propose a model that contemplates the action of Salmonella SraL sRNA in the protection of rho mRNA from premature transcription termination by Rho. Note that since the interaction region between both RNAs corresponds to a very-well-conserved sequence, it is plausible to admit that this regulation also occurs in other enterobacteria.
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12

King, Rodney A., and Robert A. Weisberg. "Suppression of Factor-Dependent TranscriptionTermination by AntiterminatorRNA." Journal of Bacteriology 185, no. 24 (December 15, 2003): 7085–91. http://dx.doi.org/10.1128/jb.185.24.7085-7091.2003.

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ABSTRACT Nascent transcripts of the phage HK022 put sites modify the transcription elongation complex so that it terminates less efficiently at intrinsic transcription terminators and accelerates through pause sites. We show here that the modification also suppresses termination in vivo at two factor-dependent terminators, one that depends on the bacterial Rho protein and a second that depends on the HK022-encoded Nun protein. Suppression was efficient when the termination factors were present at physiological levels, but an increase in the intracellular concentration of Nun increased termination both in the presence and absence of put. put-mediated antitermination thus shows no apparent terminator specificity, suggesting that put inhibits a step that is common to termination at the different types of terminator.
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13

Seoh, Hyuk Kyu, Michelle Weech, Ning Zhang, and Catherine L. Squires. "rRNA Antitermination Functions with Heat Shock Promoters." Journal of Bacteriology 185, no. 21 (November 1, 2003): 6486–89. http://dx.doi.org/10.1128/jb.185.21.6486-6489.2003.

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ABSTRACT Transcription antitermination in the rRNA operons of Escherichia coli requires a unique nucleic acid sequence that serves as a signal for modification of the elongating RNA polymerase, making it resistant to Rho-dependent termination. We examined the antitermination ability of RNA polymerase elongation complexes that had initiated at three different heat shock promoters, dnaK, groE, and clpB, and then transcribed the antitermination sequence to read through a Rho-dependent terminator. Terminator bypass comparable to that seen with σ70 promoters was obtained. Lack of or inversion of the sequence abolished terminator readthrough. We conclude that RNA polymerase that uses σ32 to initiate transcription can adopt a conformation similar to that of σ70-containing RNA polymerase, enabling it to interact with auxiliary modifying proteins and bypass Rho-dependent terminators.
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14

Epshtein, Vitaly, Dipak Dutta, Joseph Wade, and Evgeny Nudler. "An allosteric mechanism of Rho-dependent transcription termination." Nature 463, no. 7278 (January 14, 2010): 245–49. http://dx.doi.org/10.1038/nature08669.

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15

Burns, Christopher M., William L. Nowatzke, and John P. Richardson. "Activation of Rho-dependent Transcription Termination by NusG." Journal of Biological Chemistry 274, no. 8 (February 19, 1999): 5245–51. http://dx.doi.org/10.1074/jbc.274.8.5245.

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16

Proshkin, Sergey, Alexander Mironov, and Evgeny Nudler. "Riboswitches in regulation of Rho-dependent transcription termination." Biochimica et Biophysica Acta (BBA) - Gene Regulatory Mechanisms 1839, no. 10 (October 2014): 974–77. http://dx.doi.org/10.1016/j.bbagrm.2014.04.002.

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17

Wang, Xun, Monford Paul Abishek N, Heung Jin Jeon, Yonho Lee, Jin He, Sankar Adhya, and Heon M. Lim. "Processing generates 3′ ends of RNA masking transcription termination events in prokaryotes." Proceedings of the National Academy of Sciences 116, no. 10 (February 19, 2019): 4440–45. http://dx.doi.org/10.1073/pnas.1813181116.

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Two kinds of signal-dependent transcription termination and RNA release mechanisms have been established in prokaryotes in vitro by: (i) binding of Rho to cytidine-rich nascent RNA [Rho-dependent termination (RDT)], and (ii) the formation of a hairpin structure in the nascent RNA, ending predominantly with uridine residues [Rho-independent termination (RIT)]. As shown here, the two signals act independently of each other and can be regulated (suppressed) by translation–transcription coupling in vivo. When not suppressed, both RIT- and RDT-mediated transcription termination do occur, but ribonucleolytic processing generates defined new 3′ ends in the terminated RNA molecules. The actual termination events at the end of transcription units are masked by generation of new processed 3′ RNA ends; thus the in vivo 3′ ends do not define termination sites. We predict generation of 3′ ends of mRNA by processing is a common phenomenon in prokaryotes as is the case in eukaryotes.
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18

Cheng, S. W., D. L. Court, and D. I. Friedman. "Transcription termination signals in the nin region of bacteriophage lambda: identification of Rho-dependent termination regions." Genetics 140, no. 3 (July 1, 1995): 875–87. http://dx.doi.org/10.1093/genetics/140.3.875.

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Abstract The approximately 3-kb nin region of bacteriophage lambda, located between genes P and Q contains transcription termination signals as well as 10 open reading frames. Deletions in the nin region frees phage growth from dependence on the lambda-encoded N-transcription antitermination system, conferring a Nin phenotype (N-independence). A subregion of nin, roc, is defined by a 1.9-kb deletion (delta roc) which partially frees lambda growth from the requirement for N antitermination. The roc region has strong transcription termination activity as assayed by a plasmid-based terminator testing system. We report the following features of the roc region: the biologically significant terminators in the roc region are Rho dependent, deletion analysis located the biologically significant termination signals to a 1.2 kb-segment of roc, and analysis of other deletions and point mutations in the roc region suggested at least two biologically significant regions of termination, tR3 (extending from bp 42020 to 42231) and tR4 (extending from bp 42630 to 42825).
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19

Epshtein, Vitaly, Dipak Dutta, Joseph Wade, and Evgeny Nudler. "Erratum: An allosteric mechanism of Rho-dependent transcription termination." Nature 466, no. 7309 (August 2010): 1006. http://dx.doi.org/10.1038/nature09360.

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20

Burova, Elena, and Max E. Gottesman. "NusG overexpression inhibits Rho-dependent termination in Escherichia coli." Molecular Microbiology 17, no. 4 (August 15, 1995): 633–41. http://dx.doi.org/10.1111/j.1365-2958.1995.mmi_17040633.x.

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21

Chae, Huiseok, Kook Han, Kwang-sun Kim, Hongmarn Park, Jungmin Lee, and Younghoon Lee. "Rho-dependent Termination ofssrS(6S RNA) Transcription inEscherichia coli." Journal of Biological Chemistry 286, no. 1 (October 29, 2010): 114–22. http://dx.doi.org/10.1074/jbc.m110.150201.

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22

Richardson, Lislott V., and John P. Richardson. "Rho-dependent Termination of Transcription Is Governed Primarily by the Upstream Rho Utilization (rut) Sequences of a Terminator." Journal of Biological Chemistry 271, no. 35 (August 30, 1996): 21597–603. http://dx.doi.org/10.1074/jbc.271.35.21597.

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23

Muteeb, Ghazala, Debashish Dey, Saurabh Mishra, and Ranjan Sen. "A multipronged strategy of an anti-terminator protein to overcome Rho-dependent transcription termination." Nucleic Acids Research 40, no. 22 (September 29, 2012): 11213–28. http://dx.doi.org/10.1093/nar/gks872.

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24

Nadiras, Cédric, Mildred Delaleau, Annie Schwartz, Emmanuel Margeat, and Marc Boudvillain. "A Fluorogenic Assay To Monitor Rho-Dependent Termination of Transcription." Biochemistry 58, no. 7 (January 9, 2019): 865–74. http://dx.doi.org/10.1021/acs.biochem.8b01216.

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25

Lau, L. F., and J. W. Roberts. "Rho-dependent transcription termination at lambda R1 requires upstream sequences." Journal of Biological Chemistry 260, no. 1 (January 1985): 574–84. http://dx.doi.org/10.1016/s0021-9258(18)89771-x.

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26

Nadiras, Cédric, Eric Eveno, Annie Schwartz, Nara Figueroa-Bossi, and Marc Boudvillain. "A multivariate prediction model for Rho-dependent termination of transcription." Nucleic Acids Research 46, no. 16 (June 21, 2018): 8245–60. http://dx.doi.org/10.1093/nar/gky563.

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27

Hussein, Razika, Tiffany Y. Lee, and Han N. Lim. "Quantitative characterization of gene regulation by Rho dependent transcription termination." Biochimica et Biophysica Acta (BBA) - Gene Regulatory Mechanisms 1849, no. 8 (August 2015): 940–54. http://dx.doi.org/10.1016/j.bbagrm.2015.05.003.

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28

Shashni, Rajesh, M. Zuhaib Qayyum, V. Vishalini, Debashish Dey, and Ranjan Sen. "Redundancy of primary RNA-binding functions of the bacterial transcription terminator Rho." Nucleic Acids Research 42, no. 15 (July 31, 2014): 9677–90. http://dx.doi.org/10.1093/nar/gku690.

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Abstract The bacterial transcription terminator, Rho, terminates transcription at half of the operons. According to the classical model derived from in vitro assays on a few terminators, Rho is recruited to the transcription elongation complex (EC) by recognizing specific sites (rut) on the nascent RNA. Here, we explored the mode of in vivo recruitment process of Rho. We show that sequence specific recognition of the rut site, in majority of the Rho-dependent terminators, can be compromised to a great extent without seriously affecting the genome-wide termination function as well as the viability of Escherichia coli. These terminators function optimally only through a NusG-assisted recruitment and activation of Rho. Our data also indicate that at these terminators, Rho-EC-bound NusG interaction facilitates the isomerization of Rho into a translocase-competent form by stabilizing the interactions of mRNA with the secondary RNA binding site, thereby overcoming the defects of the primary RNA binding functions.
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29

Jin, D. J., R. R. Burgess, J. P. Richardson, and C. A. Gross. "Termination efficiency at rho-dependent terminators depends on kinetic coupling between RNA polymerase and rho." Proceedings of the National Academy of Sciences 89, no. 4 (February 15, 1992): 1453–57. http://dx.doi.org/10.1073/pnas.89.4.1453.

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30

Carrano, Lucia, Cecilia Bucci, Roberto De Pascalis, Alfredo Lavitola, Filomena Manna, Emiliana Corti, Carmelo Bruno Bruni, and Pietro Alifano. "Effects of Bicyclomycin on RNA- and ATP-Binding Activities of Transcription Termination Factor Rho." Antimicrobial Agents and Chemotherapy 42, no. 3 (March 1, 1998): 571–78. http://dx.doi.org/10.1128/aac.42.3.571.

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ABSTRACT Bicyclomycin is a commercially important antibiotic that has been shown to be effective against many gram-negative bacteria. Genetic and biochemical evidence indicates that the antibiotic interferes with RNA metabolism in Escherichia coli by inhibiting the activity of transcription termination factor Rho. However, the precise mechanism of inhibition is not completely known. In this study we have used in vitro transcription assays to analyze the effects of bicyclomycin on the termination step of transcription. The Rho-dependent transcription termination region located within thehisG cistron of Salmonella typhimurium has been used as an experimental system. The possible interference of the antibiotic with the various functions of factor Rho, such as RNA binding at the primary site, ATP binding, and hexamer formation, has been investigated by RNA gel mobility shift, photochemical cross-linking, and gel filtration experiments. The results of these studies demonstrate that bicyclomycin does not interfere with the binding of Rho to the loading site on nascent RNA. Binding of the factor to ATP is not impeded, on the contrary, the antibiotic appears to decrease the apparent equilibrium dissociation constant for ATP in photochemical cross-linking experiments. The available evidence suggests that this decrease might be due to an interference with the correct positioning of ATP within the nucleotide-binding pocket leading b an inherent block of ATP hydrolysis. Possibly, as a consequence of this interference, the antibiotic also prevents ATP-dependent stabilization of Rho hexamers.
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31

Morgan, William, David G. Bear, Bronwen L. Litchman, and Peter H. von Hippel. "RNA sequence and secondary structure requiresments for rho-dependent transcription termination." Nucleic Acids Research 13, no. 10 (1985): 3739–54. http://dx.doi.org/10.1093/nar/13.10.3739.

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32

Chen, C. Y., and J. P. Richardson. "Sequence elements essential for rho-dependent transcription termination at lambda tR1." Journal of Biological Chemistry 262, no. 23 (August 1987): 11292–99. http://dx.doi.org/10.1016/s0021-9258(18)60958-5.

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33

Madden, Kathleen A., and Arthur Landy. "Rho-dependent transcription termination in the tyrT operon of Escherichia coli." Gene 76, no. 2 (March 1989): 271–80. http://dx.doi.org/10.1016/0378-1119(89)90167-4.

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34

Figueroa-Bossi, N., A. Schwartz, B. Guillemardet, F. D'Heygere, L. Bossi, and M. Boudvillain. "RNA remodeling by bacterial global regulator CsrA promotes Rho-dependent transcription termination." Genes & Development 28, no. 11 (June 1, 2014): 1239–51. http://dx.doi.org/10.1101/gad.240192.114.

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35

Zheng, C., and D. I. Friedman. "Reduced Rho-dependent transcription termination permits NusA-independent growth of Escherichia coli." Proceedings of the National Academy of Sciences 91, no. 16 (August 2, 1994): 7543–47. http://dx.doi.org/10.1073/pnas.91.16.7543.

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36

D'Heygère, François, Annie Schwartz, Franck Coste, Bertrand Castaing, and Marc Boudvillain. "ATP-dependent motor activity of the transcription termination factor Rho fromMycobacterium tuberculosis." Nucleic Acids Research 43, no. 12 (May 20, 2015): 6099–111. http://dx.doi.org/10.1093/nar/gkv505.

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37

Krypotou, Emilia, Guy E. Townsend, Xiaohui Gao, Shoichi Tachiyama, Jun Liu, Nick D. Pokorzynski, Andrew L. Goodman, and Eduardo A. Groisman. "Bacteria require phase separation for fitness in the mammalian gut." Science 379, no. 6637 (March 17, 2023): 1149–56. http://dx.doi.org/10.1126/science.abn7229.

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Therapeutic manipulation of the gut microbiota holds great potential for human health. The mechanisms bacteria use to colonize the gut therefore present valuable targets for clinical intervention. We now report that bacteria use phase separation to enhance fitness in the mammalian gut. We establish that the intrinsically disordered region (IDR) of the broadly and highly conserved transcription termination factor Rho is necessary and sufficient for phase separation in vivo and in vitro in the human commensal Bacteroides thetaiotaomicron . Phase separation increases transcription termination by Rho in an IDR-dependent manner. Moreover, the IDR is critical for gene regulation in the gut. Our findings expose phase separation as vital for host-commensal bacteria interactions and relevant for novel clinical applications.
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38

Konan, Kouacou Vincent, and Charles Yanofsky. "Rho-Dependent Transcription Termination in the tnaOperon of Escherichia coli: Roles of the boxASequence and the rut Site." Journal of Bacteriology 182, no. 14 (July 15, 2000): 3981–88. http://dx.doi.org/10.1128/jb.182.14.3981-3988.2000.

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ABSTRACT Expression of the tryptophanase (tna) operon ofEscherichia coli is regulated by catabolite repression and by tryptophan-induced transcription antitermination. Tryptophan induction prevents Rho-dependent transcription termination in the leader region of the operon. Induction requires translation of a 24-residue leader peptide-coding region, tnaC, containing a single, crucial Trp codon. Studies with a lacZ reporter construct lacking the tnaC-tnaA spacer region suggest that, in the presence of excess tryptophan, the TnaC leader peptide acts incis on the ribosome translating tnaC to inhibit its release. The stalled ribosome is thought to block Rho's access to the transcript. In this paper we examine the roles of theboxA sequence and the rut site in Rho-dependent termination. Deleting six nucleotides (CGC CCT) of boxA or introducing specific point mutations in boxA results in high-level constitutive expression. Some constitutive changes introduced in boxA do not change the TnaC peptide sequence. We confirm that deletion of the rut site results in constitutive expression. We also demonstrate that, in each constitutive construct, replacement of the tnaC start codon by a UAG stop codon reduces expression significantly, suggesting that constitutive expression requires translation of the tnaCcoding sequence. Addition of bicyclomycin, an inhibitor of Rho, to these UAG constructs increases expression, demonstrating that reduced expression is due to Rho action. Combining a boxA point mutation with rut site deletion results in constitutive expression comparable to that of a maximally induced operon. These results support the hypothesis that in the presence of tryptophan the ribosome translating tnaC blocks Rho's access to theboxA and rut sites, thereby preventing transcription termination.
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39

Ranjan, Amitabh, Savita Sharma, Ramanuj Banerjee, Udayaditya Sen, and Ranjan Sen. "Structural and mechanistic basis of anti-termination of Rho-dependent transcription termination by bacteriophage P4 capsid protein Psu." Nucleic Acids Research 41, no. 14 (May 22, 2013): 6839–56. http://dx.doi.org/10.1093/nar/gkt336.

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40

Bastet, Laurène, Adrien Chauvier, Navjot Singh, Antony Lussier, Anne-Marie Lamontagne, Karine Prévost, Eric Massé, Joseph T. Wade, and Daniel A. Lafontaine. "Translational control and Rho-dependent transcription termination are intimately linked in riboswitch regulation." Nucleic Acids Research 45, no. 12 (May 18, 2017): 7474–86. http://dx.doi.org/10.1093/nar/gkx434.

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41

Rivellini, F., P. Alifano, C. Piscitelli, V. Blasi, C. B. Brunt, and M. S. Carlomagno. "A cytosine- over guanosine-rich sequence in RNA activates rho-dependent transcription termination." Molecular Microbiology 5, no. 12 (December 1991): 3049–54. http://dx.doi.org/10.1111/j.1365-2958.1991.tb01864.x.

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42

Pani, Bibhusita, Sharmistha Banerjee, Jisha Chalissery, Muralimohan Abishek, Ramya Malarini Loganathan, Ragan Babu Suganthan, and Ranjan Sen. "Mechanism of Inhibition of Rho-dependent Transcription Termination by Bacteriophage P4 Protein Psu." Journal of Biological Chemistry 281, no. 36 (July 7, 2006): 26491–500. http://dx.doi.org/10.1074/jbc.m603982200.

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43

Roberts, Elizabeth A., Theresa L. Eisenbraun, Christopher L. Andrews, and David G. Bear. "3'-End formation at the phage .lambda. tR1 .rho.-dependent transcription termination site." Biochemistry 30, no. 22 (June 1991): 5429–37. http://dx.doi.org/10.1021/bi00236a015.

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44

Pani, Bibhusita, Sharmistha Banerjee, Jisha Chalissery, Abishek Muralimohan, Ramya Malarini Loganathan, Ragan Babu Suganthan, and Ranjan Sen. "Mechanism of inhibition of Rho-dependent transcription termination by bacteriophage P4 protein Psu." Journal of Biological Chemistry 284, no. 37 (September 4, 2009): 25459.4–25459. http://dx.doi.org/10.1074/jbc.a603982200.

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45

Valabhoju, Vishalini, Sonia Agrawal, and Ranjan Sen. "Molecular Basis of NusG-mediated Regulation of Rho-dependent Transcription Termination in Bacteria." Journal of Biological Chemistry 291, no. 43 (September 7, 2016): 22386–403. http://dx.doi.org/10.1074/jbc.m116.745364.

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46

Briani, Federica, Sandro Zangrossi, Daniela Ghisotti, and GIANNI Dehò. "A Rho-Dependent Transcription Termination Site Regulated by Bacteriophage P4 RNA Immunity Factor." Virology 223, no. 1 (September 1996): 57–67. http://dx.doi.org/10.1006/viro.1996.0455.

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47

Wang, Xun, Sang Chun Ji, Heung Jin Jeon, Yonho Lee, and Heon M. Lim. "Two-level inhibition of galK expression by Spot 42: Degradation of mRNA mK2 and enhanced transcription termination before the galK gene." Proceedings of the National Academy of Sciences 112, no. 24 (June 4, 2015): 7581–86. http://dx.doi.org/10.1073/pnas.1424683112.

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Abstract:
The Escherichia coli gal operon has the structure Pgal-galE-galT-galK-galM. During early log growth, a gradient in gene expression, named type 2 polarity, is established, as follows: galE > galT > galK > galM. However, during late-log growth, type 1 polarity is established in which galK is greater than galT, as follows: galE > galK > galT > galM. We found that type 2 polarity occurs as a result of the down-regulation of galK, which is caused by two different molecular mechanisms: Spot 42-mediated degradation of the galK-specific mRNA, mK2, and Spot 42-mediated Rho-dependent transcription termination at the end of galT. Because the concentration of Spot 42 drops during the transition period of the polarity type switch, these results demonstrate that type 1 polarity is the result of alleviation of Spot 42-mediated galK down-regulation. Because the Spot 42-binding site overlaps with a putative Rho-binding site, a molecular mechanism is proposed to explain how Spot 42, possibly with Hfq, enhances Rho-mediated transcription termination at the end of galT.
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48

Yakhnin, Helen, Joshua E. Babiarz, Alexander V. Yakhnin, and Paul Babitzke. "Expression of the Bacillus subtilis trpEDCFBAOperon Is Influenced by Translational Coupling and Rho Termination Factor." Journal of Bacteriology 183, no. 20 (October 15, 2001): 5918–26. http://dx.doi.org/10.1128/jb.183.20.5918-5926.2001.

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ABSTRACT The trp RNA-binding attenuation protein (TRAP) regulates expression of the Bacillus subtilis trpEDCFBAoperon by transcription attenuation and translational control mechanisms. Both mechanisms require binding of tryptophan-activated TRAP to 11 (G/U)AG repeats in the trp leader transcript.trpE translational control involves formation of a TRAP-dependent RNA structure that sequesters the trpEShine-Dalgarno (SD) sequence (the SD blocking hairpin). By comparing expression levels fromtrpE′-′lacZ translational fusions controlled by the wild-type leader or by a leader that cannot form the SD blocking hairpin, we found that translational control requires a tryptophan concentration higher than that required for transcription attenuation. We also found that inhibition oftrpE translation by the SD blocking hairpin does not alter the stability of the downstream message. Since the coding sequences for trpE and trpD overlap by 29 nucleotides, we examined expression levels fromtrpED′-′lacZ translational fusions to determine if these two genes are translationally coupled. We found that introduction of a UAA stop codon in trpEresulted in a substantial reduction in expression. Since expression was partially restored in the presence of a tRNA suppressor, our results indicate that trpE and trpD are translationally coupled. We determined that the coupling mechanism is TRAP independent and that formation of the SD blocking hairpin regulates trpD translation via translational coupling. We also constructed a rho mutation to investigate the role of Rho-dependent termination in trp operon expression. We found that TRAP-dependent formation of the SD blocking hairpin allows Rho access to the nascent transcript, causing transcriptional polarity.
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49

Pasman, Zvi, and Peter H. von Hippel. "Regulation of Rho-Dependent Transcription Termination by NusG Is Specific to theEscherichia coliElongation Complex†." Biochemistry 39, no. 18 (May 2000): 5573–85. http://dx.doi.org/10.1021/bi992658z.

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50

Hart, C. M., and J. W. Roberts. "Rho-dependent transcription termination. Characterization of the requirement for cytidine in the nascent transcript." Journal of Biological Chemistry 266, no. 35 (December 1991): 24140–48. http://dx.doi.org/10.1016/s0021-9258(18)54405-7.

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