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Journal articles on the topic 'RecFOR'

Author: Grafiati

Published: 6 September 2023

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1

Morimatsu, Katsumi, Yun Wu, and Stephen C. Kowalczykowski. "RecFOR Proteins Target RecA Protein to a DNA Gap with Either DNA or RNA at the 5′ Terminus." Journal of Biological Chemistry 287, no. 42 (August 17, 2012): 35621–30. http://dx.doi.org/10.1074/jbc.m112.397034.

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The repair of single-stranded gaps in duplex DNA by homologous recombination requires the proteins of the RecF pathway. The assembly of RecA protein onto gapped DNA (gDNA) that is complexed with the single-stranded DNA-binding protein is accelerated by the RecF, RecO, and RecR (RecFOR) proteins. Here, we show the RecFOR proteins specifically target RecA protein to gDNA even in the presence of a thousand-fold excess of single-stranded DNA (ssDNA). The binding constant of RecF protein, in the presence of the RecOR proteins, to the junction of ssDNA and dsDNA within a gap is 1–2 nm, suggesting that a few RecF molecules in the cell are sufficient to recognize gDNA. We also found that the nucleation of a RecA filament on gDNA in the presence of the RecFOR proteins occurs at a faster rate than filament elongation, resulting in a RecA nucleoprotein filament on ssDNA for 1000–2000 nucleotides downstream (5′ → 3′) of the junction with duplex DNA. Thus, RecA loading by RecFOR is localized to a region close to a junction. RecFOR proteins also recognize RNA at the 5′-end of an RNA-DNA junction within an ssDNA gap, which is compatible with their role in the repair of lagging strand gaps at stalled replication forks.

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2

Che, Shiyou, Yujing Chen, Yakun Liang, Qionglin Zhang, and Mark Bartlam. "Crystal structure of RecR, a member of the RecFOR DNA-repair pathway, fromPseudomonas aeruginosaPAO1." Acta Crystallographica Section F Structural Biology Communications 74, no. 4 (March 22, 2018): 222–30. http://dx.doi.org/10.1107/s2053230x18003503.

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DNA damage is usually lethal to all organisms. Homologous recombination plays an important role in the DNA damage-repair process in prokaryotic organisms. Two pathways are responsible for homologous recombination inPseudomonas aeruginosa: the RecBCD pathway and the RecFOR pathway. RecR is an important regulator in the RecFOR homologous recombination pathway inP. aeruginosa. It forms complexes with RecF and RecO that can facilitate the loading of RecA onto ssDNA in the RecFOR pathway. Here, the crystal structure of RecR fromP. aeruginosaPAO1 (PaRecR) is reported.PaRecR crystallizes in space groupP6122, with two monomers per asymmetric unit. Analytical ultracentrifugation data show thatPaRecR forms a stable dimer, but can exist as a tetramer in solution. The crystal structure shows that dimericPaRecR forms a ring-like tetramer architectureviacrystal symmetry. The presence of a ligand in the Walker B motif of one RecR subunit suggests a putative nucleotide-binding site.

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3

Ivančić-Baće, Ivana, Petra Peharec, Sunčana Moslavac, Nikolina Škrobot, Erika Salaj-Šmic†, and Krunoslav Brčić-Kostić. "RecFOR Function Is Required for DNA Repair and Recombination in a RecA Loading-Deficient recB Mutant of Escherichia coli." Genetics 163, no. 2 (February 1, 2003): 485–94. http://dx.doi.org/10.1093/genetics/163.2.485.

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Abstract The RecA loading activity of the RecBCD enzyme, together with its helicase and 5′ → 3′ exonuclease activities, is essential for recombination in Escherichia coli. One particular mutant in the nuclease catalytic center of RecB, i.e., recB1080, produces an enzyme that does not have nuclease activity and is unable to load RecA protein onto single-stranded DNA. There are, however, previously published contradictory data on the recombination proficiency of this mutant. In a recF– background the recB1080 mutant is recombination deficient, whereas in a recF+ genetic background it is recombination proficient. A possible explanation for these contrasting phenotypes may be that the RecFOR system promotes RecA-single-strand DNA filament formation and replaces the RecA loading defect of the RecB1080CD enzyme. We tested this hypothesis by using three in vivo assays. We compared the recombination proficiencies of recB1080, recO, recR, and recF single mutants and recB1080 recO, recB1080 recR, and recB1080 recF double mutants. We show that RecFOR functions rescue the repair and recombination deficiency of the recB1080 mutant and that RecA loading is independent of RecFOR in the recB1080 recD double mutant where this activity is provided by the RecB1080C(D–) enzyme. According to our results as well as previous data, three essential activities for the initiation of recombination in the recB1080 mutant are provided by different proteins, i.e., helicase activity by RecB1080CD, 5′ → 3′ exonuclease by RecJ- and RecA-single-stranded DNA filament formation by RecFOR.

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4

Sakai, Akiko, and Michael M. Cox. "RecFOR and RecOR as Distinct RecA Loading Pathways." Journal of Biological Chemistry 284, no. 5 (November 4, 2008): 3264–72. http://dx.doi.org/10.1074/jbc.m807220200.

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5

Zahradka, Ksenija, Jelena Repar, Damir Đermić, and Davor Zahradka. "Genetic analysis of transductional recombination in Escherichia coli reveals differences in the postsynaptic stages of RecBCD and RecFOR pathways." Periodicum Biologorum 124, no. 3-4 (May 5, 2023): 97–106. http://dx.doi.org/10.18054/pb.v124i3-4.23604.

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Background and purpose: Homologous recombination in Escherichia coli proceeds via two pathways, RecBCD and RecFOR, which use different enzymes for DNA end resection and loading of RecA recombinase. The postsynaptic reactions following RecA-mediated homologous pairing have mostly been studied within the RecBCD pathway. They involve RuvABC helicase/resolvase complex, RecG and RadA helicases that process recombination intermediates to produce recombinant DNA molecules. Also, RecG functionally interacts with the PriA protein in initiation of recombination-dependent replication. Here, we studied the individual and combined effects of ruvABC, recG and radA null mutations on transductional recombination in both pathways. The effect of the priA300 mutation, which acts as a suppressor of the recG mutation, was also tested. The goal was to characterize the postsynaptic stage of transductional recombination in more details, especially in the RecFOR pathway, which is less well-studied. Materials and methods: Phage P1vir-mediated transduction was used to measure recombination efficiency in a series of recombination mutants. The proA+ marker was used for selection in transductional crosses with various ΔproA recipients. Results: The ruvABC mutation moderately decreased recombination in both recombination pathways, while radA had no effect. The recG mutation reduced recombination in the RecBCD pathway but not in the RecFOR pathway. The strong recombination defect of recG radA double mutants in both pathways was completely suppressed by the priA300 mutation, and this suppression depended on the functional RuvABC complex. Conclusions: RecG and RadA proteins have a redundant role in transductional recombination via RecFOR pathway. In both recombination pathways, RecG and RadA functionally interact with PriA, probably during initiation of recombination-dependent replication.

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6

Handa, Naofumi, Asao Ichige, and Ichizo Kobayashi. "Contribution of RecFOR machinery of homologous recombination to cell survival after loss of a restriction–modification gene complex." Microbiology 155, no. 7 (July 1, 2009): 2320–32. http://dx.doi.org/10.1099/mic.0.026401-0.

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Loss of a type II restriction–modification (RM) gene complex, such as EcoRI, from a bacterial cell leads to death of its descendent cells through attack by residual restriction enzymes on undermethylated target sites of newly synthesized chromosomes. Through such post-segregational host killing, these gene complexes impose their maintenance on their host cells. This finding led to the rediscovery of type II RM systems as selfish mobile elements. The host prokaryote cells were found to cope with such attacks through a variety of means. The RecBCD pathway of homologous recombination in Escherichia coli repairs the lethal lesions on the chromosome, whilst it destroys restricted non-self DNA. recBCD homologues, however, appear very limited in distribution among bacterial genomes, whereas homologues of the RecFOR proteins, responsible for another pathway, are widespread in eubacteria, just like the RM systems. In the present work, therefore, we examined the possible contribution of the RecFOR pathway to cell survival after loss of an RM gene complex. A recF mutation reduced survival in an otherwise rec-positive background and, more severely, in a recBC sbcBC background. We also found that its effect is prominent in the presence of specific non-null mutant forms of the RecBCD enzyme: the resistance to killing seen with recC1002, recC1004, recC2145 and recB2154 is severely reduced to the level of a null recBC allele when combined with a recF, recO or recR mutant allele. Such resistance was also dependent on RecJ and RecQ functions. UV resistance of these non-null recBCD mutants is also reduced by recF, recJ or recQ mutation. These results demonstrate that the RecFOR pathway of recombination can contribute greatly to resistance to RM-mediated host killing, depending on the genetic background.

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7

Anand, Syam P., Haocheng Zheng, Piero R. Bianco, Sanford H. Leuba, and Saleem A. Khan. "DNA Helicase Activity of PcrA Is Not Required for the Displacement of RecA Protein from DNA or Inhibition of RecA-Mediated Strand Exchange." Journal of Bacteriology 189, no. 12 (April 20, 2007): 4502–9. http://dx.doi.org/10.1128/jb.00376-07.

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ABSTRACT PcrA is a conserved DNA helicase present in all gram-positive bacteria. Bacteria lacking PcrA show high levels of recombination. Lethality induced by PcrA depletion can be overcome by suppressor mutations in the recombination genes recFOR. RecFOR proteins load RecA onto single-stranded DNA during recombination. Here we test whether an essential function of PcrA is to interfere with RecA-mediated DNA recombination in vitro. We demonstrate that PcrA can inhibit the RecA-mediated DNA strand exchange reaction in vitro. Furthermore, PcrA displaced RecA from RecA nucleoprotein filaments. Interestingly, helicase mutants of PcrA also displaced RecA from DNA and inhibited RecA-mediated DNA strand exchange. Employing a novel single-pair fluorescence resonance energy transfer-based assay, we demonstrate a lengthening of double-stranded DNA upon polymerization of RecA and show that PcrA and its helicase mutants can reverse this process. Our results show that the displacement of RecA from DNA by PcrA is not dependent on its translocase activity. Further, our results show that the helicase activity of PcrA, although not essential, might play a facilitatory role in the RecA displacement reaction.

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8

Ivančić-Baće, Ivana, Erika Salaj-Šmic, and Krunoslav Brčić-Kostić. "Effects of recJ, recQ, and recFOR Mutations on Recombination in Nuclease-Deficient recB recD Double Mutants of Escherichia coli." Journal of Bacteriology 187, no. 4 (February 15, 2005): 1350–56. http://dx.doi.org/10.1128/jb.187.4.1350-1356.2005.

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ABSTRACT The two main recombination pathways in Escherichia coli (RecBCD and RecF) have different recombination machineries that act independently in the initiation of recombination. Three essential enzymatic activities are required for early recombinational processing of double-stranded DNA ends and breaks: a helicase, a 5′→3′ exonuclease, and loading of RecA protein onto single-stranded DNA tails. The RecBCD enzyme performs all of these activities, whereas the recombination machinery of the RecF pathway consists of RecQ (helicase), RecJ (5′→3′ exonuclease), and RecFOR (RecA-single-stranded DNA filament formation). The recombination pathway operating in recB (nuclease-deficient) mutants is a hybrid because it includes elements of both the RecBCD and RecF recombination machineries. In this study, genetic analysis of recombination in a recB (nuclease-deficient) recD double mutant was performed. We show that conjugational recombination and DNA repair after UV and gamma irradiation in this mutant are highly dependent on recJ, partially dependent on recFOR, and independent of recQ. These results suggest that the recombination pathway operating in a nuclease-deficient recB recD double mutant is also a hybrid. We propose that the helicase and RecA loading activities belong to the RecBCD recombination machinery, while the RecJ-mediated 5′→3′ exonuclease is an element of the RecF recombination machinery.

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9

Ivančić-Baće, Ivana, Ignacija Vlašić, Erika Salaj-Šmic, and Krunoslav Brčić-Kostić. "Genetic Evidence for the Requirement of RecA Loading Activity in SOS Induction after UV Irradiation in Escherichia coli." Journal of Bacteriology 188, no. 14 (July 15, 2006): 5024–32. http://dx.doi.org/10.1128/jb.00130-06.

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ABSTRACT The SOS response in Escherichia coli results in the coordinately induced expression of more than 40 genes which occurs when cells are treated with DNA-damaging agents. This response is dependent on RecA (coprotease), LexA (repressor), and the presence of single-stranded DNA (ssDNA). A prerequisite for SOS induction is the formation of a RecA-ssDNA filament. Depending on the DNA substrate, the RecA-ssDNA filament is produced by either RecBCD, RecFOR, or a hybrid recombination mechansim with specific enzyme activities, including helicase, exonuclease, and RecA loading. In this study we examined the role of RecA loading activity in SOS induction after UV irradiation. We performed a genetic analysis of SOS induction in strains with a mutation which eliminates RecA loading activity in the RecBCD enzyme (recB1080 allele). We found that RecA loading activity is essential for SOS induction. In the recB1080 mutant RecQ helicase is not important, whereas RecJ nuclease slightly decreases SOS induction after UV irradiation. In addition, we found that the recB1080 mutant exhibited constitutive expression of the SOS regulon. Surprisingly, this constitutive SOS expression was dependent on the RecJ protein but not on RecFOR, implying that there is a different mechanism of RecA loading for constitutive SOS expression.

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10

Lee, Su-jin, Si Yeon Ahn, Han Byeol Oh, Seung Yeon Kim, Wan Seok Song, and Sung-il Yoon. "Structural and Biochemical Analysis of the Recombination Mediator Protein RecR from Campylobacter jejuni." International Journal of Molecular Sciences 24, no. 16 (August 18, 2023): 12947. http://dx.doi.org/10.3390/ijms241612947.

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The recombination mediator complex RecFOR, consisting of the RecF, RecO, and RecR proteins, is needed to initiate homologous recombination in bacteria by positioning the recombinase protein RecA on damaged DNA. Bacteria from the phylum Campylobacterota, such as the pathogen Campylobacter jejuni, lack the recF gene and trigger homologous recombination using only RecR and RecO. To elucidate the functional properties of C. jejuni RecR (cjRecR) in recombination initiation that differ from or are similar to those in RecF-expressing bacteria, we determined the crystal structure of cjRecR and performed structure-based binding analyses. cjRecR forms a rectangular ring-like tetrameric structure and coordinates a zinc ion using four cysteine residues, as observed for RecR proteins from RecF-expressing bacteria. However, the loop of RecR that has been shown to recognize RecO and RecF in RecF-expressing bacteria is substantially shorter in cjRecR as a canonical feature of Campylobacterota RecR proteins, indicating that cjRecR lost a part of the loop in evolution due to the lack of RecF and has a low RecO-binding affinity. Furthermore, cjRecR features a larger positive patch and exhibits substantially higher ssDNA-binding affinity than RecR from RecF-expressing bacteria. Our study provides a framework for a deeper understanding of the RecOR-mediated recombination pathway.

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11

Lestini, Roxane, and Bénédicte Michel. "UvrD and UvrD252 Counteract RecQ, RecJ, and RecFOR in a rep Mutant of Escherichia coli." Journal of Bacteriology 190, no. 17 (June 20, 2008): 5995–6001. http://dx.doi.org/10.1128/jb.00620-08.

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ABSTRACT Rep and UvrD are two related Escherichia coli helicases, and inactivating both is lethal. Based on the observation that the synthetic lethality of rep and uvrD inactivation is suppressed in the absence of the recombination presynaptic proteins RecF, RecO, or RecR, it was proposed that UvrD is essential in the rep mutant to counteract a deleterious RecFOR-dependent RecA binding. We show here that the synthetic lethality of rep and uvrD mutations is also suppressed by recQ and recJ inactivation but not by rarA inactivation. Furthermore, it is independent of the action of UvrD in nucleotide excision repair and mismatch repair. These observations support the idea that UvrD counteracts a deleterious RecA binding to forks blocked in the rep mutant. An ATPase-deficient mutant of UvrD [uvrD(R284A)] is dominant negative in a rep mutant, but only in the presence of all RecQJFOR proteins, suggesting that the UvrD(R284A) mutant protein is deleterious when it counteracts one of these proteins. In contrast, the uvrD252 mutant (G30D), which exhibits a strongly decreased ATPase activity, is viable in a rep mutant, where it allows replication fork reversal. We conclude that the residual ATPase activity of UvrD252 prevents a negative effect on the viability of the rep mutant and allows UvrD to counteract the action of RecQ, RecJ, and RecFOR at forks blocked in the rep mutant. Models for the action of UvrD at blocked forks are proposed.

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12

Grompone, Gianfranco, Nicolas Sanchez, S. Dusko Ehrlich, and Bénédicte Michel. "Requirement for RecFOR-mediated recombination in priA mutant." Molecular Microbiology 52, no. 2 (March 19, 2004): 551–62. http://dx.doi.org/10.1111/j.1365-2958.2004.03997.x.

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13

Satoh, Katsuya, Masahiro Kikuchi, Abu M. Ishaque, Hirofumi Ohba, Mitsugu Yamada, Kouhei Tejima, Takefumi Onodera, and Issay Narumi. "The role of Deinococcus radiodurans RecFOR proteins in homologous recombination." DNA Repair 11, no. 4 (April 2012): 410–18. http://dx.doi.org/10.1016/j.dnarep.2012.01.008.

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14

Buljubašić, Maja, Ana Hlevnjak, Jelena Repar, Damir Đermić, Vedrana Filić, Igor Weber, Ksenija Zahradka, and Davor Zahradka. "RecBCD- RecFOR-independent pathway of homologous recombination in Escherichia coli." DNA Repair 83 (November 2019): 102670. http://dx.doi.org/10.1016/j.dnarep.2019.102670.

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15

Wang, Yuan, Guangzhi Xu, Liangyan Wang, and Yuejin Hua. "Distinct roles of Deinococcus radiodurans RecFOR and RecA in DNA transformation." Biochemical and Biophysical Research Communications 513, no. 3 (June 2019): 740–45. http://dx.doi.org/10.1016/j.bbrc.2019.04.042.

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16

Fujii, Shingo, Asako Isogawa, and Robert P. Fuchs. "RecFOR proteins are essential for Pol V-mediated translesion synthesis and mutagenesis." EMBO Journal 25, no. 24 (November 30, 2006): 5754–63. http://dx.doi.org/10.1038/sj.emboj.7601474.

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17

Chaudhary, Santosh Kumar, Mohanapriya Elayappan, Jeyaraman Jeyakanthan, and Sekar Kanagaraj. "Structural and functional characterization of oligomeric states of proteins in RecFOR pathway." International Journal of Biological Macromolecules 163 (November 2020): 943–53. http://dx.doi.org/10.1016/j.ijbiomac.2020.07.062.

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18

Morimatsu, Katsumi, and Stephen C. Kowalczykowski. "RecFOR Proteins Load RecA Protein onto Gapped DNA to Accelerate DNA Strand Exchange." Molecular Cell 11, no. 5 (May 2003): 1337–47. http://dx.doi.org/10.1016/s1097-2765(03)00188-6.

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19

Lia, Giuseppe, Annafrancesca Rigato, Emilie Long, Carine Chagneau, Marie Le Masson, Jean-François Allemand, and Bénédicte Michel. "RETRACTED: RecA-Promoted, RecFOR-Independent Progressive Disassembly of Replisomes Stalled by Helicase Inactivation." Molecular Cell 49, no. 3 (February 2013): 547–57. http://dx.doi.org/10.1016/j.molcel.2012.11.018.

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20

Espinosa-Aguirre, Javier, Claudia Barajas-Lemus, Sandra Hernández-Ojeda, Tzipe Govezensky, Julieta Rubio, and Rafael Camacho-Carranza. "RecBCD and RecFOR dependent induction of chromosomal deletions by sodium selenite in Salmonella." Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis 665, no. 1-2 (June 2009): 14–19. http://dx.doi.org/10.1016/j.mrfmmm.2009.02.012.

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21

Henrikus, Sarah S., Camille Henry, Harshad Ghodke, Elizabeth A. Wood, Neema Mbele, Roopashi Saxena, Upasana Basu, Antoine M. van Oijen, Michael M. Cox, and Andrew Robinson. "RecFOR epistasis group: RecF and RecO have distinct localizations and functions inEscherichia coli." Nucleic Acids Research 47, no. 6 (January 18, 2019): 2946–65. http://dx.doi.org/10.1093/nar/gkz003.

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22

Maxwell, K. L., P. Reed, R. g. Zhang, S. Beasley, A. R. Walmsley, F. A. Curtis, A. Joachimiak, A. M. Edwards, and G. J. Sharples. "Functional similarities between phage Orf and Escherichia coli RecFOR in initiation of genetic exchange." Proceedings of the National Academy of Sciences 102, no. 32 (August 2, 2005): 11260–65. http://dx.doi.org/10.1073/pnas.0503399102.

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23

Rangarajan, Savithri, Roger Woodgate, and Myron F. Goodman. "Replication restart in UV-irradiatedEscherichia coliinvolving pols II, III, V, PriA, RecA and RecFOR proteins." Molecular Microbiology 43, no. 3 (February 2002): 617–28. http://dx.doi.org/10.1046/j.1365-2958.2002.02747.x.

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24

Raychaudhury, Paromita, and Kenneth J. Marians. "The recombination mediator proteins RecFOR maintain RecA* levels for maximal DNA polymerase V Mut activity." Journal of Biological Chemistry 294, no. 3 (November 27, 2018): 852–60. http://dx.doi.org/10.1074/jbc.ra118.005726.

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25

Lia, Giuseppe, Annafrancesca Rigato, Emilie Long, Carine Chagneau, Marie Le Masson, Jean-François Allemand, and Bénédicte Michel. "Retraction Notice to: RecA-Promoted, RecFOR-Independent Progressive Disassembly of Replisomes Stalled by Helicase Inactivation." Molecular Cell 54, no. 3 (May 2014): 537. http://dx.doi.org/10.1016/j.molcel.2014.04.019.

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26

Peng, Lang, Rexford Mawunyo Dumevi, Marco Chitto, Nadja Haarmann, Petya Berger, Gerald Koudelka, Herbert Schmidt, Alexander Mellmann, Ulrich Dobrindt, and Michael Berger. "A Robust One-Step Recombineering System for Enterohemorrhagic Escherichia coli." Microorganisms 10, no. 9 (August 23, 2022): 1689. http://dx.doi.org/10.3390/microorganisms10091689.

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Enterohemorrhagic Escherichia coli (EHEC) can cause severe diarrheic in humans. To improve therapy options, a better understanding of EHEC pathogenicity is essential. The genetic manipulation of EHEC with classical one-step methods, such as the transient overexpression of the phage lambda (λ) Red functions, is not very efficient. Here, we provide a robust and reliable method for increasing recombineering efficiency in EHEC based on the transient coexpression of recX together with gam, beta, and exo. We demonstrate that the genetic manipulation is 3–4 times more efficient in EHEC O157:H7 EDL933 Δstx1/2 with our method when compared to the overexpression of the λ Red functions alone. Both recombineering systems demonstrated similar efficiencies in Escherichia coli K-12 MG1655. Coexpression of recX did not enhance the Gam-mediated inhibition of sparfloxacin-mediated SOS response. Therefore, the additional inhibition of the RecFOR pathway rather than a stronger inhibition of the RecBCD pathway of SOS response induction might have resulted in the increased recombineering efficiency by indirectly blocking phage induction. Even though additional experiments are required to unravel the precise mechanistic details of the improved recombineering efficiency, we recommend the use of our method for the robust genetic manipulation of EHEC and other prophage-carrying E. coli isolates.

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Li, Shisheng, and Raymond Waters. "Escherichia coli Strains Lacking Protein HU Are UV Sensitive due to a Role for HU in Homologous Recombination." Journal of Bacteriology 180, no. 15 (August 1, 1998): 3750–56. http://dx.doi.org/10.1128/jb.180.15.3750-3756.1998.

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ABSTRACT hupA and hupB encode the α and β subunits of the Escherichia coli histone-like protein HU. Here we show that E. coli hup mutants are sensitive to UV in the rec+ sbc +, recBC sbcA, recBC sbcBC, umuDC,recF, and recD backgrounds. However,hupAB mutations do not enhance the UV sensitivity of resolvase-deficient recG ruvA strains. hupAB uvrA and hupAB recG strains are supersensitive to UV.hup mutations enhance the UV sensitivity ofruvA strains to a much lesser extent but enhance that ofrus-1 ruvA strains to the same extent as forrus+ ruv + strains. Our results suggest that HU plays a role in recombinational DNA repair that is not specifically limited to double-strand break repair or daughter strand gap repair; the lack of HU affects the RecG RusA and RuvABC pathways for Holliday junction processing equally if the two pathways are equally active in recombinational repair; the function of HU is not in the substrate processing step or in the RecFOR-directed synapsis action during recombinational repair. Furthermore, the UV sensitivity ofhup mutants cannot be suppressed by overexpression of wild-type or mutant gyrB, which confers novobiocin resistance, or by different concentrations of a gyrase inhibitor that can increase or decrease the supercoiling of chromosomal DNA.

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28

Centore, Richard C., and Steven J. Sandler. "UvrD Limits the Number and Intensities of RecA-Green Fluorescent Protein Structures in Escherichia coli K-12." Journal of Bacteriology 189, no. 7 (January 26, 2007): 2915–20. http://dx.doi.org/10.1128/jb.01777-06.

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ABSTRACT RecA is important for recombination, DNA repair, and SOS induction. In Escherichia coli, RecBCD, RecFOR, and RecJQ prepare DNA substrates onto which RecA binds. UvrD is a 3′-to-5′ helicase that participates in methyl-directed mismatch repair and nucleotide excision repair. uvrD deletion mutants are sensitive to UV irradiation, hypermutable, and hyper-rec. In vitro, UvrD can dissociate RecA from single-stranded DNA. Other experiments suggest that UvrD removes RecA from DNA where it promotes unproductive reactions. To test if UvrD limits the number and/or the size of RecA-DNA structures in vivo, an uvrD mutation was combined with recA-gfp. This recA allele allows the number of RecA structures and the amount of RecA at these structures to be assayed in living cells. uvrD mutants show a threefold increase in the number of RecA-GFP foci, and these foci are, on average, nearly twofold higher in relative intensity. The increased number of RecA-green fluorescent protein foci in the uvrD mutant is dependent on recF, recO, recR, recJ, and recQ. The increase in average relative intensity is dependent on recO and recQ. These data support an in vivo role for UvrD in removing RecA from the DNA.

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29

Aono, Shelly, Thomas Hartsch, and Ursula Schulze-Gahmen. "Crystallization of a member of the recFOR DNA repair pathway, RecO, with and without bound oligonucleotide." Acta Crystallographica Section D Biological Crystallography 59, no. 3 (February 21, 2003): 576–79. http://dx.doi.org/10.1107/s0907444903000428.

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30

Laureti, Luisa, Lara Lee, Gaëlle Philippin, Michel Kahi, and Vincent Pagès. "Single strand gap repair: The presynaptic phase plays a pivotal role in modulating lesion tolerance pathways." PLOS Genetics 18, no. 6 (June 2, 2022): e1010238. http://dx.doi.org/10.1371/journal.pgen.1010238.

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During replication, the presence of unrepaired lesions results in the formation of single stranded DNA (ssDNA) gaps that need to be repaired to preserve genome integrity and cell survival. All organisms have evolved two major lesion tolerance pathways to continue replication: Translesion Synthesis (TLS), potentially mutagenic, and Homology Directed Gap Repair (HDGR), that relies on homologous recombination. In Escherichia coli, the RecF pathway repairs such ssDNA gaps by processing them to produce a recombinogenic RecA nucleofilament during the presynaptic phase. In this study, we show that the presynaptic phase is crucial for modulating lesion tolerance pathways since the competition between TLS and HDGR occurs at this stage. Impairing either the extension of the ssDNA gap (mediated by the nuclease RecJ and the helicase RecQ) or the loading of RecA (mediated by RecFOR) leads to a decrease in HDGR and a concomitant increase in TLS. Hence, we conclude that defects in the presynaptic phase delay the formation of the D-loop and increase the time window allowed for TLS. In contrast, we show that a defect in the postsynaptic phase that impairs HDGR does not lead to an increase in TLS. Unexpectedly, we also reveal a strong genetic interaction between recF and recJ genes, that results in a recA deficient-like phenotype in which HDGR is almost completely abolished.

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Zuñiga-Castillo, Jacobo, David Romero, and Jaime M. Martínez-Salazar. "The Recombination Genes addAB Are Not Restricted to Gram-Positive Bacteria: Genetic Analysis of the Recombination Initiation Enzymes RecF and AddAB in Rhizobium etli." Journal of Bacteriology 186, no. 23 (December 1, 2004): 7905–13. http://dx.doi.org/10.1128/jb.186.23.7905-7913.2004.

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ABSTRACT Single-strand gaps (SSGs) and double-strand breaks (DSBs) are the major initiation sites for recombination. In bacteria, the SSGs are repaired by RecFOR, while the DSBs are processed by RecBCD in gram-negative bacteria and AddAB in gram-positive bacteria. Unexpectedly, instead of recBCD genes, the addAB genes were found in members of the α-proteobacteria group (gram negative). Taking Rhizobium etli as a model, the role of recF and addAB genes in homologous recombination and repair of damaged DNA was evaluated. Inactivation of either recF or addA provoked strong sensitivity to UV radiation and mitomycin C, while an additive effect was observed in the recF-addA mutant. The DSBs generated by nalidixic acid caused low viability only in the addA mutant. The recombination frequency of large and small plasmids was reduced in the recF mutant (24- and 36-fold, respectively), whereas a slight decrease (threefold) in the addA mutant was observed. Moreover, an additive effect (47- and 90-fold, respectively) was observed in the double mutant, but it was not as dramatic as that in a recA mutant. Interestingly, the frequency of deletion and Campbell-type recombination was slightly affected in either single or double mutants. These results suggest that another pathway exists that allows plasmid and Campbell-type recombination in the absence of recF and addA genes.

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Prahlad, Janani, Yifeng Yuan, Jiusheng Lin, Chou-Wei Chang, Dirk Iwata-Reuyl, Yilun Liu, Valérie de Crécy-Lagard, and Mark A. Wilson. "The DUF328 family member YaaA is a DNA-binding protein with a novel fold." Journal of Biological Chemistry 295, no. 41 (August 12, 2020): 14236–47. http://dx.doi.org/10.1074/jbc.ra120.015055.

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DUF328 family proteins are present in many prokaryotes; however, their molecular activities are unknown. The Escherichia coli DUF328 protein YaaA is a member of the OxyR regulon and is protective against oxidative stress. Because uncharacterized proteins involved in prokaryotic oxidative stress response are rare, we sought to learn more about the DUF328 family. Using comparative genomics, we found a robust association between the DUF328 family and genes involved in DNA recombination and the oxidative stress response. In some proteins, DUF328 domains are fused to other domains involved in DNA binding, recombination, and repair. Cofitness analysis indicates that DUF328 family genes associate with recombination-mediated DNA repair pathways, particularly the RecFOR pathway. Purified recombinant YaaA binds to dsDNA, duplex DNA containing bubbles of unpaired nucleotides, and Holliday junction constructs in vitro with dissociation equilibrium constants of 200–300 nm. YaaA binds DNA with positive cooperativity, forming multiple shifted species in electrophoretic mobility shift assays. The 1.65-Å resolution X-ray crystal structure of YaaA reveals that the protein possesses a new fold that we name the cantaloupe fold. YaaA has a positively charged cleft and a helix-hairpin-helix DNA-binding motif found in other DNA repair enzymes. Our results demonstrate that YaaA is a new type of DNA-binding protein associated with the oxidative stress response and that this molecular function is likely conserved in other DUF328 family members.

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Bhattacharya, Resham, and Doris J. Beck. "Survival and SOS induction in cisplatin-treated Escherichia coli deficient in Pol II, RecBCD and RecFOR functions." DNA Repair 1, no. 11 (November 2002): 955–66. http://dx.doi.org/10.1016/s1568-7864(02)00147-7.

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Putteet-Driver, Adrienne D., Jianmin Zhong, and Alan G. Barbour. "Transgenic Expression of RecA of the Spirochetes Borrelia burgdorferi and Borrelia hermsii in Escherichia coli Revealed Differences in DNA Repair and Recombination Phenotypes." Journal of Bacteriology 186, no. 8 (April 15, 2004): 2266–74. http://dx.doi.org/10.1128/jb.186.8.2266-2274.2004.

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ABSTRACT After unsuccessful attempts to recover a viable RecA-deficient mutant of the Lyme borreliosis agent Borrelia burgdorferi, we characterized the functional activities of RecA of B. burgdorferi, as well as RecA of the relapsing fever spirochete Borrelia hermsii and the free-living spirochete Leptospira biflexa, in a recA mutant of Escherichia coli. As a control, E. coli RecA was expressed from the same plasmid vector. DNA damage repair activity was assessed after exposure of the transgenic cells to UV light or the radiomimetic chemicals methyl methanesulfonate and mitomycin C. Recombination activity in the cells was assessed by using an assay for homologous recombination between repeats in the chromosome and by measuring the ability of the cells to foster lytic growth by red gam mutant bacteriophage λ. Overall, we found that transgenic cells with recA genes of B. burgdorferi, B. hermsii, and L. biflexa had approximately equivalent activities in promoting homologous recombination in the lacZ duplication assay, but cells with B. burgdorferi recA and, most notably, B. hermsii recA were significantly less capable than cells with L. biflexa recA or E. coli recA in responding to DNA damage or in facilitating plaque formation in the phage assay. The comparatively poor function of Borrelia recA in the latter set of assays may be the consequence of impaired coordination in the loading of the transgenic RecA by RecBCD and/or RecFOR in E. coli.

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Belle, Jerilyn J., Andrew Casey, Charmain T. Courcelle, and Justin Courcelle. "Inactivation of the DnaB Helicase Leads to the Collapse and Degradation of the Replication Fork: a Comparison to UV-Induced Arrest." Journal of Bacteriology 189, no. 15 (May 25, 2007): 5452–62. http://dx.doi.org/10.1128/jb.00408-07.

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ABSTRACT Replication forks face a variety of structurally diverse impediments that can prevent them from completing their task. The mechanism by which cells overcome these hurdles is likely to vary depending on the nature of the obstacle and the strand in which the impediment is encountered. Both UV-induced DNA damage and thermosensitive replication proteins have been used in model systems to inhibit DNA replication and characterize the mechanism by which it recovers. In this study, we examined the molecular events that occur at replication forks following inactivation of a thermosensitive DnaB helicase and found that they are distinct from those that occur following arrest at UV-induced DNA damage. Following UV-induced DNA damage, the integrity of replication forks is maintained and protected from extensive degradation by RecA, RecF, RecO, and RecR until replication can resume. By contrast, inactivation of DnaB results in extensive degradation of the nascent and leading-strand template DNA and a loss of replication fork integrity as monitored by two-dimensional agarose gel analysis. The degradation that occurs following DnaB inactivation partially depends on several genes, including recF, recO, recR, recJ, recG, and xonA. Furthermore, the thermosensitive DnaB allele prevents UV-induced DNA degradation from occurring following arrest even at the permissive temperature, suggesting a role for DnaB prior to loading of the RecFOR proteins. We discuss these observations in relation to potential models for both UV-induced and DnaB(Ts)-mediated replication inhibition.

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Bentchikou, Esma, Pascale Servant, Geneviève Coste, and Suzanne Sommer. "A Major Role of the RecFOR Pathway in DNA Double-Strand-Break Repair through ESDSA in Deinococcus radiodurans." PLoS Genetics 6, no. 1 (January 15, 2010): e1000774. http://dx.doi.org/10.1371/journal.pgen.1000774.

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Gupta, Richa, Stewart Shuman, and Michael S. Glickman. "RecF and RecR Play Critical Roles in the Homologous Recombination and Single-Strand Annealing Pathways of Mycobacteria." Journal of Bacteriology 197, no. 19 (July 20, 2015): 3121–32. http://dx.doi.org/10.1128/jb.00290-15.

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ABSTRACTMycobacteria encode three DNA double-strand break repair pathways: (i) RecA-dependent homologous recombination (HR), (ii) Ku-dependent nonhomologous end joining (NHEJ), and (iii) RecBCD-dependent single-strand annealing (SSA). Mycobacterial HR has two presynaptic pathway options that rely on the helicase-nuclease AdnAB and the strand annealing protein RecO, respectively. Ablation ofadnABorrecOindividually causes partial impairment of HR, but loss ofadnABandrecOin combination abolishes HR. RecO, which can accelerate annealing of single-stranded DNAin vitro, also participates in the SSA pathway. The functions of RecF and RecR, which, in other model bacteria, function in concert with RecO as mediators of RecA loading, have not been examined in mycobacteria. Here, we present a genetic analysis ofrecFandrecRin mycobacterial recombination. We find that RecF, like RecO, participates in the AdnAB-independent arm of the HR pathway and in SSA. In contrast, RecR is required for all HR in mycobacteria and for SSA. The essentiality of RecR as an agent of HR is yet another distinctive feature of mycobacterial DNA repair.IMPORTANCEThis study clarifies the molecular requirements for homologous recombination in mycobacteria. Specifically, we demonstrate that RecF and RecR play important roles in both the RecA-dependent homologous recombination and RecA-independent single-strand annealing pathways. Coupled with our previous findings (R. Gupta, M. Ryzhikov, O. Koroleva, M. Unciuleac, S. Shuman, S. Korolev, and M. S. Glickman, Nucleic Acids Res 41:2284–2295, 2013,http://dx.doi.org/10.1093/nar/gks1298), these results revise our view of mycobacterial recombination and place the RecFOR system in a central position in homology-dependent DNA repair.

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Zahradka, Ksenija, Sanela Šimić, Maja Buljubašić, Mirjana Petranović, Damir Đermić, and Davor Zahradka. "sbcB15 and ΔsbcB Mutations Activate Two Types of RecF Recombination Pathways in Escherichia coli." Journal of Bacteriology 188, no. 21 (August 25, 2006): 7562–71. http://dx.doi.org/10.1128/jb.00613-06.

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ABSTRACT Escherichia coli cells with mutations in recBC genes are defective for the main RecBCD pathway of recombination and have severe reductions in conjugational and transductional recombination, as well as in recombinational repair of double-stranded DNA breaks. This phenotype can be corrected by suppressor mutations in sbcB and sbcC(D) genes, which activate an alternative RecF pathway of recombination. It was previously suggested that sbcB15 and ΔsbcB mutations, both of which inactivate exonuclease I, are equally efficient in suppressing the recBC phenotype. In the present work we reexamined the effects of sbcB15 and ΔsbcB mutations on DNA repair after UV and γ irradiation, on conjugational recombination, and on the viability of recBC (sbcC) cells. We found that the sbcB15 mutation is a stronger recBC suppressor than ΔsbcB, suggesting that some unspecified activity of the mutant SbcB15 protein may be favorable for recombination in the RecF pathway. We also showed that the xonA2 mutation, a member of another class of ExoI mutations, had the same effect on recombination as ΔsbcB, suggesting that it is an sbcB null mutation. In addition, we demonstrated that recombination in a recBC sbcB15 sbcC mutant is less affected by recF and recQ mutations than recombination in recBC ΔsbcB sbcC and recBC xonA2 sbcC strains is, indicating that SbcB15 alleviates the requirement for the RecFOR complex and RecQ helicase in recombination processes. Our results suggest that two types of sbcB-sensitive RecF pathways can be distinguished in E. coli, one that is activated by the sbcB15 mutation and one that is activated by sbcB null mutations. Possible roles of SbcB15 in recombination reactions in the RecF pathway are discussed.

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Zahradka, Ksenija, Jelena Repar, Damir Đermić, and Davor Zahradka. "Chromosome Segregation and Cell Division Defects in Escherichia coli Recombination Mutants Exposed to Different DNA-Damaging Treatments." Microorganisms 11, no. 3 (March 9, 2023): 701. http://dx.doi.org/10.3390/microorganisms11030701.

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Homologous recombination repairs potentially lethal DNA lesions such as double-strand DNA breaks (DSBs) and single-strand DNA gaps (SSGs). In Escherichia coli, DSB repair is initiated by the RecBCD enzyme that resects double-strand DNA ends and loads RecA recombinase to the emerging single-strand (ss) DNA tails. SSG repair is mediated by the RecFOR protein complex that loads RecA onto the ssDNA segment of gaped duplex. In both repair pathways, RecA catalyses reactions of homologous DNA pairing and strand exchange, while RuvABC complex and RecG helicase process recombination intermediates. In this work, we have characterised cytological changes in various recombination mutants of E. coli after three different DNA-damaging treatments: (i) expression of I-SceI endonuclease, (ii) γ-irradiation, and (iii) UV-irradiation. All three treatments caused severe chromosome segregation defects and DNA-less cell formation in the ruvABC, recG, and ruvABC recG mutants. After I-SceI expression and γ-irradiation, this phenotype was efficiently suppressed by the recB mutation, indicating that cytological defects result mostly from incomplete DSB repair. In UV-irradiated cells, the recB mutation abolished cytological defects of recG mutants and also partially suppressed the cytological defects of ruvABC recG mutants. However, neither recB nor recO mutation alone could suppress the cytological defects of UV-irradiated ruvABC mutants. The suppression was achieved only by simultaneous inactivation of the recB and recO genes. Cell survival and microscopic analysis suggest that chromosome segregation defects in UV-irradiated ruvABC mutants largely result from defective processing of stalled replication forks. The results of this study show that chromosome morphology is a valuable marker in genetic analyses of recombinational repair in E. coli.

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Jain, Kanika, Elizabeth A. Wood, and Michael M. Cox. "The rarA gene as part of an expanded RecFOR recombination pathway: Negative epistasis and synthetic lethality with ruvB, recG, and recQ." PLOS Genetics 17, no. 12 (December 22, 2021): e1009972. http://dx.doi.org/10.1371/journal.pgen.1009972.

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The RarA protein, homologous to human WRNIP1 and yeast MgsA, is a AAA+ ATPase and one of the most highly conserved DNA repair proteins. With an apparent role in the repair of stalled or collapsed replication forks, the molecular function of this protein family remains obscure. Here, we demonstrate that RarA acts in late stages of recombinational DNA repair of post-replication gaps. A deletion of most of the rarA gene, when paired with a deletion of ruvB or ruvC, produces a growth defect, a strong synergistic increase in sensitivity to DNA damaging agents, cell elongation, and an increase in SOS induction. Except for SOS induction, these effects are all suppressed by inactivating recF, recO, or recJ, indicating that RarA, along with RuvB, acts downstream of RecA. SOS induction increases dramatically in a rarA ruvB recF/O triple mutant, suggesting the generation of large amounts of unrepaired ssDNA. The rarA ruvB defects are not suppressed (and in fact slightly increased) by recB inactivation, suggesting RarA acts primarily downstream of RecA in post-replication gaps rather than in double strand break repair. Inactivating rarA, ruvB and recG together is synthetically lethal, an outcome again suppressed by inactivation of recF, recO, or recJ. A rarA ruvB recQ triple deletion mutant is also inviable. Together, the results suggest the existence of multiple pathways, perhaps overlapping, for the resolution or reversal of recombination intermediates created by RecA protein in post-replication gaps within the broader RecF pathway. One of these paths involves RarA.

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Johnston, Calum, Isabelle Mortier-Barrière, Chantal Granadel, Patrice Polard, Bernard Martin, and Jean-Pierre Claverys. "RecFOR Is Not Required for Pneumococcal Transformation but Together with XerS for Resolution of Chromosome Dimers Frequently Formed in the Process." PLoS Genetics 11, no. 1 (January 8, 2015): e1004934. http://dx.doi.org/10.1371/journal.pgen.1004934.

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Lee, Byung Il, Kyoung Hoon Kim, Sun Mi Shim, Kyung Soo Ha, Jin Kuk Yang, Hye-Jin Yoon, Jun Yong Ha, and Se Won Suh. "Crystallization and preliminary X-ray crystallographic analysis of the RecR protein fromDeinococcus radiodurans, a member of the RecFOR DNA-repair pathway." Acta Crystallographica Section D Biological Crystallography 60, no. 2 (January 24, 2004): 379–81. http://dx.doi.org/10.1107/s0907444903028191.

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Moore, T. "The RdgC protein of Escherichia coli binds DNA and counters a toxic effect of RecFOR in strains lacking the replication restart protein PriA." EMBO Journal 22, no. 3 (February 3, 2003): 735–45. http://dx.doi.org/10.1093/emboj/cdg048.

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Pollard, L. M., Y. K. Chutake, P. M. Rindler, and S. I. Bidichandani. "Deficiency of RecA-dependent RecFOR and RecBCD pathways causes increased instability of the (GAA{middle dot}TTC)n sequence when GAA is the lagging strand template." Nucleic Acids Research 35, no. 20 (November 29, 2007): 6884–94. http://dx.doi.org/10.1093/nar/gkm810.

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Keller, Kimberly L., Terri L. Overbeck-Carrick, and Doris J. Beck. "Survival and induction of SOS in Escherichia coli treated with cisplatin, UV-irradiation, or mitomycin C are dependent on the function of the RecBC and RecFOR pathways of homologous recombination." Mutation Research/DNA Repair 486, no. 1 (June 2001): 21–29. http://dx.doi.org/10.1016/s0921-8777(01)00077-5.

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46

Neborsky, E. V. "THE RECTOR’s H-INDEX AS A FACTOR OF DEVELOPMENT OF UNIVERSITY SCIENTIFIC CAPACITY." Вестник Удмуртского университета. Социология. Политология. Международные отношения 3, no. 2 (June 25, 2019): 123–30. http://dx.doi.org/10.35634/2587-9030-2019-3-2-123-130.

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The strategic development of universities in the modern world is determined, among other things, by their scientific achievements. The purpose of this study was to classify the patterns between the h -index of a rector and the scientific potential of a university, expressed by the i -index. The sample consisted of 100 Russian universities. The results of the study are grouped into four types, connecting the characteristics of management at the university with the h-index of its rector: “rector-administrator”, “rector-manager”, “rector-authority”, “rector-researcher”. The two most common types in the sample were “rector-manager” and “rector-researcher”. In the first case, the h -index of a rector is lower than 10 points, and the i -index of a corresponding university is equal to or higher than 10 points. There are 40 such cases in the sample of 100. In the second case, the h -index of a rector is equal to or higher than 10 points, and the university’s i -index is also equal to or higher than 10 points. There are 41 such cases in the sample of 100. In 14 cases, the h -index of a rector is higher than the i -index of a corresponding university.

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Moreno, Manuel. "Visión de la educación a distancia en México. Entrevista al Dr. Francisco Cervantes, Rector de la UnADM." Revista Mexicana de Bachillerato a Distancia 7, no. 14 (August 31, 2015): 4. http://dx.doi.org/10.22201/cuaed.20074751e.2015.14.65262.

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<p>Interesante entrevista al doctor Francisco Cervantes, Rector de la UnADM, sobre la Visión de la educación a distancia en México, realizada por el maestro Manuel Moreno, Rector del Sistema de Universidad Virtual de la UDG.</p>

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Maroco dos Santos, Emanuel José. "La universidad vista por Unamuno: las funciones del rector y de los claustros." Ideas y Valores 67, no. 166 (January 4, 2018): 233–42. http://dx.doi.org/10.15446/ideasyvalores.v67n166.53913.

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El hecho de que Unamuno sea un escritor autobiográfico nos permite determinar su concepción de rector, no solo sobre la base de lo que nos dice acerca de dicho cargo, sino también a partir de su experiencia, lo que es particularmente sugestivo, ya que la idea sui generis que tenía de dicho cargo se encarna en la realidad social que lo rodea.Por ejemplo, un texto que permitiría acceder a la experiencia de Unamuno como rector esel discurso que pronunció en el “Paraninfo de la Universidadde Salamanca el 1 de octubre de 1931, al inaugurar, en calidad de rector, el curso académico de 1931-1932” (cf. Unamuno 1971d 395).

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Dodi Suswandi, Ivan Hanfi, and Muhammad Yusro. "Information System Planning Integrated database of training in food and nutrition at SEAMEO RECFON Using Togaf Architecture." Journal of Scientific Research, Education, and Technology (JSRET) 2, no. 2 (June 6, 2023): 687–706. http://dx.doi.org/10.58526/jsret.v2i2.143.

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Southeast Asian Ministers of Education Organization Regional Center for Food and Nutrition (SEAMEO RECFON), is an organization of Southeast Asian ministers of education that focuses on food and nutrition. Currently, the application of SI / IT in the SEAMEO RECFON environment is not optimal, referring to the data base system that has not been integrated so that data and information exchange is not effective, the SI / IT investment made has also not given a good return, the training program in the field of food and nutrition each year is consistently not optimal, and several performance indicators are found not to meet their targets. Therefore, enterprise architecture planning is needed at SEAMEO RECFON which aims to formulate the principles and fundamentals of SEAMEO RECFON in accordance with the direction of its goals so as to produce healthy business processes, systems that can support training activities in the fields of food and nutrition, operations and infrastructure that can support the system to run well. This enterprise architecture planning is made using TOGAF (The Open Group of Architecture Framework) version 9.2 with the ADM (Architecture Development Method) method. This enterprise architecture planning produces a map of the main activities and support for food and nutrition training at SEAMEO RECFON, stakeholders, their focus, business objectives and basic principles, blueprints for business architecture targets, information systems architecture, technology architecture, and application implementation roadmap.

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Yuliana, Vera, and Etmi Hardi. "Z Mawardi Effendi: Perjalanan Karir Seorang Akademisi dan Mantan Rektor Universitas Negeri Padang Dua Periode (1975-2020)." Jurnal Kronologi 3, no. 3 (August 26, 2021): 272–85. http://dx.doi.org/10.24036/jk.v3i3.195.

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This research aims to provide an overview of the life and career journey of Z Mawardi Effendi and his role in leading the State University of Padang as rector of two periods. Therefore, the first stage is to collect data from oral and written sources. The second stage is the criticism of sources both internal and external sources. Next, the third stage is the analysis and interpretation of data. Lastly, the fourth stage is to describe the results of research in the form of scientific writing in accordance with the rules of historical research. The conclusion of this study is that Z Mawardi Effendi is an academic figure from Koto Panjang, Tanah Datar and has a career at Padang State University for approximately 50 years. He started his career as a young lecturer in 1975 and briefly served several administrative roles continuously ranging from Head of Learning Resources Center, Vice Dean, Dean, Vice Rector, to the highest administrative position in a university, namely Rector. Not only that, after serving as Rector, he also held other positions such as Chairman of Postgraduate Program and Chairman of The Senate of Padang State University. The position continued until the end of retirement so that it has many roles for the State University of Padang. Keywords: Biography, Figure, Education, Lecturer, Rector

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