A Life Investigating Pathways That Repair Broken Chromosomes

Haber, James E.

doi:10.1146/annurev-genet-120215-035043

Cited by 86 publications

(92 citation statements)

References 164 publications

(136 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…1]. Normally, HO endonuclease is expressed at the end of G1, after passage through “start,” but cells have entered S phase before recombination has been completed (Haber 2016). However, MAT switching can be induced both in cells arrested and maintained prior to S phase, when Cdc7 is inactivated (Hicks et al 2011), or in G2/M-arrested cells (Wang et al 2004), by expressing the HO endonuclease gene under control of a galactose-inducible promoter.…”

Section: A Different Mechanism For the Directionality Of Mating-type mentioning

confidence: 99%

Mating-type switching by homology-directed recombinational repair: a matter of choice

et al. 2018

Self Cite

View full text Add to dashboard Cite

In eukaryotes, all DNA transactions happen in the context of chromatin that often takes part in regulatory mechanisms. In particular, chromatin structure can regulate exchanges of DNA occurring through homologous recombination. Few systems have provided as detailed a view on this phenomenon as mating-type switching in yeast. Mating-type switching entails the choice of a template for the gene conversions of the expressed mating-type locus. In the fission yeast Schizosaccharomyces pombe, correct template choice requires two competing small recombination enhancers, SRE2 and SRE3, that function in the context of heterochromatin. These two enhancers act with the Swi2/Swi5 recombination accessory complex to initiate strand exchange in a cell-type-specific manner, from SRE2 in M cells and SRE3 in P cells. New research indicates that the Set1C complex, responsible for H3K4 methylation, and the Brl2 ubiquitin ligase, that catalyzes H2BK119 ubiquitylation, participate in the cell-type-specific selection of SRE2 or SRE3. Here, we review these findings, compare donor preference in S. pombe to the distantly related budding yeast Saccharomyces cerevisiae, and contrast the positive effects of heterochromatin on the donor selection process with other situations, where heterochromatin represses recombination.

show abstract

Section: A Different Mechanism For the Directionality Of Mating-type mentioning

confidence: 99%

Mating-type switching by homology-directed recombinational repair: a matter of choice

et al. 2018

Self Cite

View full text Add to dashboard Cite

show abstract

“…The deciphering of species-specific patterns of codon usage has effectively paved the way for the enhancement of heterologous gene translation in several model and non-model organisms 29 , 30 . Comparative assessments of codon usage patterns are important for understanding patterns of codon preferences.…”

Section: Resultsmentioning

confidence: 99%

ChloroMitoCU: Codon patterns across organelle genomes for functional genomics and evolutionary applications

et al. 2017

View full text Add to dashboard Cite

Organelle genomes are widely thought to have arisen from reduction events involving cyanobacterial and archaeal genomes, in the case of chloroplasts, or α-proteobacterial genomes, in the case of mitochondria. Heterogeneity in base composition and codon preference has long been the subject of investigation of topics ranging from phylogenetic distortion to the design of overexpression cassettes for transgenic expression. From the overexpression point of view, it is critical to systematically analyze the codon usage patterns of the organelle genomes. In light of the importance of codon usage patterns in the development of hyper-expression organelle transgenics, we present ChloroMitoCU, the first-ever curated, web-based reference catalog of the codon usage patterns in organelle genomes. ChloroMitoCU contains the pre-compiled codon usage patterns of 328 chloroplast genomes (29,960 CDS) and 3,502 mitochondrial genomes (49,066 CDS), enabling genome-wide exploration and comparative analysis of codon usage patterns across species. ChloroMitoCU allows the phylogenetic comparison of codon usage patterns across organelle genomes, the prediction of codon usage patterns based on user-submitted transcripts or assembled organelle genes, and comparative analysis with the pre-compiled patterns across species of interest. ChloroMitoCU can increase our understanding of the biased patterns of codon usage in organelle genomes across multiple clades. ChloroMitoCU can be accessed at: http://chloromitocu.cgu.edu.tw/

show abstract

“…This mechanism (one specific example of which is illustrated in Fig 8), parallels the model for base-substitution and indel formation (one indel version shown in Fig 7). Dissociation of the primer end with Pol I attached might be achieved if the editing function of Pol I is activated by the mismatch at ROS damaged bases, for example at an 8-oxo-dG:C base pair, causing dissociation of the 3'-end to enable it to attain the nuclease domain [89]. Such dissociation would permit polymerase template switching (Fig 8E), the postulated first step in microhomology-mediated recombination.…”

Section: Discussionmentioning

confidence: 99%

Persistent damaged bases in DNA allow mutagenic break repair in Escherichia coli

et al. 2017

View full text Add to dashboard Cite

Bacteria, yeast and human cancer cells possess mechanisms of mutagenesis upregulated by stress responses. Stress-inducible mutagenesis potentially accelerates adaptation, and may provide important models for mutagenesis that drives cancers, host pathogen interactions, antibiotic resistance and possibly much of evolution generally. In Escherichia coli repair of double-strand breaks (DSBs) becomes mutagenic, using low-fidelity DNA polymerases under the control of the SOS DNA-damage response and RpoS general stress response, which upregulate and allow the action of error-prone DNA polymerases IV (DinB), II and V to make mutations during repair. Pol IV is implied to compete with and replace high-fidelity DNA polymerases at the DSB-repair replisome, causing mutagenesis. We report that up-regulated Pol IV is not sufficient for mutagenic break repair (MBR); damaged bases in the DNA are also required, and that in starvation-stressed cells, these are caused by reactive-oxygen species (ROS). First, MBR is reduced by either ROS-scavenging agents or constitutive activation of oxidative-damage responses, both of which reduce cellular ROS levels. The ROS promote MBR other than by causing DSBs, saturating mismatch repair, oxidizing proteins, or inducing the SOS response or the general stress response. We find that ROS drive MBR through oxidized guanines (8-oxo-dG) in DNA, in that overproduction of a glycosylase that removes 8-oxo-dG from DNA prevents MBR. Further, other damaged DNA bases can substitute for 8-oxo-dG because ROS-scavenged cells resume MBR if either DNA pyrimidine dimers or alkylated bases are induced. We hypothesize that damaged bases in DNA pause the replisome and allow the critical switch from high fidelity to error-prone DNA polymerases in the DSB-repair replisome, thus allowing MBR. The data imply that in addition to the indirect stress-response controlled switch to MBR, a direct cis-acting switch to MBR occurs independently of DNA breakage, caused by ROS oxidation of DNA potentially regulated by ROS regulators.

show abstract

A Life Investigating Pathways That Repair Broken Chromosomes

Cited by 86 publications

References 164 publications

Mating-type switching by homology-directed recombinational repair: a matter of choice

Mating-type switching by homology-directed recombinational repair: a matter of choice

ChloroMitoCU: Codon patterns across organelle genomes for functional genomics and evolutionary applications

Persistent damaged bases in DNA allow mutagenic break repair in Escherichia coli

Contact Info

Product

Resources

About