scholarly journals Nucleogenesis and origin of organelles

2008 ◽  
Vol 16 (3-4) ◽  
pp. 88-92
Author(s):  
Milanko Stupar
Keyword(s):  
Replication Fork ◽  
Genome Duplication ◽  
Genetic Recombination ◽  
Mitochondrial Gene ◽  
Strand Break ◽  
Monophyletic Origin ◽  
Double Stranded Dna ◽  
Rigid Cell Wall ◽  
Step Mechanism ◽  
Archaeal Ancestor

Division of the ancestral prokaryotic pragenome into two circular double-stranded DNA molecules by genetic recombination is a base for the future separate evolution of the nuclear and mitochondrial gene compartment. This suggests monophyletic origin of both mitochondrion and nucleus. Presumed organism which genome undergoes genetic recombination has to be searched among an aerobic, oxygen non-producing archaeon with no rigid cell wall, but a plasma membrane. Plastids evolve from an aerobic, oxygen producing proto-eukaryot, after mitoplastide genome duplication and subsequent functional segregation. In this proposal, origin of eukaryots occurs by a three-step mechanism. First, replication fork pauses and collapses generating a breakage in the genome of archaeal ancestor of eukaryots. Second, the double-strand break can be repaired intergenomically by complementary strands invasion. Third, this duplicated genome can be fissioned into two compartments by reciprocal genetic recombination. Scenario is accomplished by aberrant fission of the inner membrane surrounding separately those two compartments.

scholarly journals Eukaryotes arose after genetic recombination

2006 ◽  
Vol 14 (1-2) ◽  
pp. 11-14 ◽  
Author(s):  
Milanko Stupar
Keyword(s):  
Cell Wall ◽  
Plasma Membrane ◽  
Genome Duplication ◽  
Genetic Recombination ◽  
Mitochondrial Gene ◽  
Dna Molecules ◽  
Monophyletic Origin ◽  
Double Stranded Dna ◽  
Rigid Cell Wall

Division of ancestral prokaryotic pragenome into two circular double-stranded DNA molecules by genetic recombination, is a base for future separate evolution of nuclear and mitochondrial gene compartment. This suggests monophyletic origin of both, mitochondrion and nucleus. Presumed organism which genome undergoes genetic recombination has to be searched among an aerobic, oxygen nonproducing, archaeon with no rigid cell wall, but a plasma membrane. Plastid evolves from an aerobic, oxygen producing protoeukaryote, after mitoplastid genome duplication and subsequent functional segregation.

scholarly journals Genome Duplication Increases Meiotic Recombination Frequency: A Saccharomyces cerevisiae Model

2020 ◽  
Author(s):  
Ou Fang ◽  
Lin Wang ◽  
Yuxin Zhang ◽  
Jixuan Yang ◽  
Qin Tao ◽  
...  
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Meiotic Recombination ◽  
Genome Stability ◽  
Genome Duplication ◽  
Genetic Recombination ◽  
Recombination Frequency ◽  
Abiotic Factors ◽  
Strand Break ◽  
Homologous Chromosomes ◽  
Almost All

Abstract Genetic recombination characterized by reciprocal exchange of genes on paired homologous chromosomes is the most prominent event in meiosis of almost all sexually reproductive organisms. It contributes to genome stability by ensuring the balanced segregation of paired homologs in meiosis, and it is also the major driving factor in generating genetic variation for natural and artificial selection. Meiotic recombination is subjected to the control of a highly stringent and complex regulating process and meiotic recombination frequency (MRF) may be affected by biological and abiotic factors such as sex, gene density, nucleotide content, and chemical/temperature treatments, having motivated tremendous researches for artificially manipulating MRF. Whether genome polyploidization would lead to a significant change in MRF has attracted both historical and recent research interests; however, tackling this fundamental question is methodologically challenging due to the lack of appropriate methods for tetrasomic genetic analysis, thus has led to controversial conclusions in the literature. This article presents a comprehensive and rigorous survey of genome duplication-mediated change in MRF using Saccharomyces cerevisiae as a eukaryotic model. It demonstrates that genome duplication can lead to consistently significant increase in MRF and rate of crossovers across all 16 chromosomes of S. cerevisiae, including both cold and hot spots of MRF. This ploidy-driven change in MRF is associated with weakened recombination interference, enhanced double-strand break density, and loosened chromatin histone occupation. The study illuminates a significant evolutionary feature of genome duplication and opens an opportunity to accelerate response to artificial and natural selection through polyploidization.

scholarly journals The Transition From Conjugal Development to the First Vegetative Cell Division Is Dependent on RAD51 Expression in the Ciliate Tetrahymena thermophila

Genetics ◽  
2001 ◽  
Vol 157 (4) ◽  
pp. 1591-1598
Author(s):  
Thomas C Marsh ◽  
Eric S Cole ◽  
Daniel P Romero
Keyword(s):  
Cell Division ◽  
Vegetative Cell ◽  
Tetrahymena Thermophila ◽  
Genetic Recombination ◽  
Reca Protein ◽  
Strand Break ◽  
Double Stranded Dna ◽  
Total Dna ◽  
Nuclear Exchange ◽  
Rdna Amplification

Abstract Rad51p, the eukaryotic homolog of the prokaryotic recA protein, catalyzes strand exchange between single- and double-stranded DNA and is involved in both genetic recombination and double-strand break repair in the ciliate Tetrahymena thermophila. We have previously shown that disruption of the Tetrahymena RAD51 somatic macronuclear locus leads to defective germline micronuclear division and that conjugation of two somatic rad51 null strains results in an early meiotic arrest. We have constructed Tetrahymena strains that are capable of RAD51 expression from their parental macronuclei and are homozygous, rad51 nulls in their germline micronuclei. These rad51 null heterokaryons complete all of the early and middle stages of conjugation, including meiosis, haploid nuclear exchange, zygotic fusion, and the programmed chromosome fragmentations, sequence eliminations, and rDNA amplification that occur during macronuclear development. However, the rad51 null progeny fail to initiate the first vegetative cell division following conjugal development. Coincident with the developmental arrest is a disproportionate amplification of rDNA, despite the maintenance of normal total DNA content in the developing macronuclei. Fusion of arrested rad51 null exconjugants to wild-type cells is sufficient to overcome the arrest. Cells rescued by cytoplasmic fusion continue to divide, eventually recapitulating the micronuclear mitotic defects described previously for rad51 somatic nulls.

scholarly journals Replication Fork Breakage and Restart inEscherichia coli

2018 ◽  
Vol 82 (3) ◽  
Author(s):  
Bénédicte Michel ◽  
Anurag K. Sinha ◽  
David R. F. Leach
Keyword(s):  
Replication Fork ◽  
Strand Break ◽  
Replication Forks ◽  
Wild Type ◽  
Dsb Repair ◽  
Replicative Helicase ◽  
Content Type ◽  
E Coli ◽  
Double Stranded Dna ◽  
Replication Restart

SUMMARYIn all organisms, replication impairments are an important source of genome rearrangements, mainly because of the formation of double-stranded DNA (dsDNA) ends at inactivated replication forks. Three reactions for the formation of dsDNA ends at replication forks were originally described forEscherichia coliand became seminal models for all organisms: the encounter of replication forks with preexisting single-stranded DNA (ssDNA) interruptions, replication fork reversal, and head-to-tail collisions of successive replication rounds. Here, we first review the experimental evidence that now allows us to know when, where, and how these three different reactions occur inE. coli. Next, we recall our recent studies showing that in wild-typeE. coli, spontaneous replication fork breakage occurs in 18% of cells at each generation. We propose that it results from the replication of preexisting nicks or gaps, since it does not involve replication fork reversal or head-to-tail fork collisions. In therecBmutant, deficient for double-strand break (DSB) repair, fork breakage triggers DSBs in the chromosome terminus during cell division, a reaction that is heritable for several generations. Finally, we recapitulate several observations suggesting that restart from intact inactivated replication forks and restart from recombination intermediates require different sets of enzymatic activities. The finding that 18% of cells suffer replication fork breakage suggests that DNA remains intact at most inactivated forks. Similarly, only 18% of cells need the helicase loader for replication restart, which leads us to speculate that the replicative helicase remains on DNA at intact inactivated replication forks and is reactivated by the replication restart proteins.

scholarly journals Focused Genetic Recombination of Bacteriophage T4 Initiated by Double-Strand Breaks

Genetics ◽  
2002 ◽  
Vol 162 (2) ◽  
pp. 543-556
Author(s):  
Victor Shcherbakov ◽  
Igor Granovsky ◽  
Lidiya Plugina ◽  
Tamara Shcherbakova ◽  
Svetlana Sizova ◽  
...  
Keyword(s):  
Genetic Recombination ◽  
Bacteriophage T4 ◽  
Proximal Part ◽  
Coupling Model ◽  
Strand Break ◽  
Double Strand Breaks ◽  
Strand Breaks ◽  
The Right ◽  
Frequency Distance

Abstract A model system for studying double-strand-break (DSB)-induced genetic recombination in vivo based on the ets1 segCΔ strain of bacteriophage T4 was developed. The ets1, a 66-bp DNA fragment of phage T2L containing the cleavage site for the T4 SegC site-specific endonuclease, was inserted into the proximal part of the T4 rIIB gene. Under segC+ conditions, the ets1 behaves as a recombination hotspot. Crosses of the ets1 against rII markers located to the left and to the right of ets1 gave similar results, thus demonstrating the equal and symmetrical initiation of recombination by either part of the broken chromosome. Frequency/distance relationships were studied in a series of two- and three-factor crosses with other rIIB and rIIA mutants (all segC+) separated from ets1 by 12-2100 bp. The observed relationships were readily interpretable in terms of the modified splice/patch coupling model. The advantages of this localized or focused recombination over that distributed along the chromosome, as a model for studying the recombination-replication pathway in T4 in vivo, are discussed.

scholarly journals PARN-like Proteins Regulate Gene Expression in Land Plant Mitochondria by Modulating mRNA Polyadenylation

2021 ◽  
Vol 22 (19) ◽  
pp. 10776
Author(s):  
Takashi Hirayama
Keyword(s):  
Mitochondrial Gene ◽  
Plant Mitochondria ◽  
Short Review ◽  
Land Plant ◽  
Mrna Processing ◽  
Regulate Gene Expression ◽  
Double Stranded Dna ◽  
Regulatory Systems ◽  
Mrna Polyadenylation

Mitochondria have their own double-stranded DNA genomes and systems to regulate transcription, mRNA processing, and translation. These systems differ from those operating in the host cell, and among eukaryotes. In recent decades, studies have revealed several plant-specific features of mitochondrial gene regulation. The polyadenylation status of mRNA is critical for its stability and translation in mitochondria. In this short review, I focus on recent advances in understanding the mechanisms regulating mRNA polyadenylation in plant mitochondria, including the role of poly(A)-specific ribonuclease-like proteins (PARNs). Accumulating evidence suggests that plant mitochondria have unique regulatory systems for mRNA poly(A) status and that PARNs play pivotal roles in these systems.

scholarly journals Strand break-induced replication fork collapse leads to C-circles, C-overhangs and telomeric recombination

PLoS Genetics ◽  
2019 ◽  
Vol 15 (2) ◽  
pp. e1007925 ◽  
Author(s):  
Tianpeng Zhang ◽  
Zepeng Zhang ◽  
Gong Shengzhao ◽  
Xiaocui Li ◽  
Haiying Liu ◽  
...  
Keyword(s):  
Replication Fork ◽  
Strand Break ◽  
Break Induced Replication

scholarly journals XLF and H2AX function in series to promote replication fork stability

2019 ◽  
Vol 218 (7) ◽  
pp. 2113-2123 ◽  
Author(s):  
Bo-Ruei Chen ◽  
Annabel Quinet ◽  
Andrea K. Byrum ◽  
Jessica Jackson ◽  
Matteo Berti ◽  
...  
Keyword(s):  
Replication Fork ◽  
Strand Break ◽  
Replication Forks ◽  
End Joining ◽  
Replication Fork Progression ◽  
In Series ◽  
Non Homologous End Joining ◽  
C Complex ◽  
Factor C ◽  
Atr Kinase

XRCC4-like factor (XLF) is a non-homologous end joining (NHEJ) DNA double strand break repair protein. However, XLF deficiency leads to phenotypes in mice and humans that are not necessarily consistent with an isolated defect in NHEJ. Here we show that XLF functions during DNA replication. XLF undergoes cell division cycle 7–dependent phosphorylation; associates with the replication factor C complex, a critical component of the replisome; and is found at replication forks. XLF deficiency leads to defects in replication fork progression and an increase in fork reversal. The additional loss of H2AX, which protects DNA ends from resection, leads to a requirement for ATR to prevent an MRE11-dependent loss of newly synthesized DNA and activation of DNA damage response. Moreover, H2ax−/−:Xlf−/− cells exhibit a marked dependence on the ATR kinase for survival. We propose that XLF and H2AX function in series to prevent replication stress induced by the MRE11-dependent resection of regressed arms at reversed replication forks.

scholarly journals Alteration of genetic recombination and double-strand break repair in human cells by progerin expression

DNA Repair ◽  
2020 ◽  
Vol 96 ◽  
pp. 102975 ◽  
Author(s):  
Celina J. Komari ◽  
Anne O. Guttman ◽  
Shelby R. Carr ◽  
Taylor L. Trachtenberg ◽  
Elise A. Orloff ◽  
...  
Keyword(s):  
Genetic Recombination ◽  
Strand Break ◽  
Double Strand Break ◽  
Human Cells ◽  
Double Strand Break Repair ◽  
Break Repair
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