scholarly journals lncRNA transcription induces meiotic recombination through chromatin remodelling in fission yeast

2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Satoshi Senmatsu ◽  
Ryuta Asada ◽  
Arisa Oda ◽  
Charles S. Hoffman ◽  
Kunihiro Ohta ◽  
...  
Keyword(s):  
Fission Yeast ◽  
Chromatin Remodeling ◽  
Meiotic Recombination ◽  
Consensus Sequence ◽  
Metabolic Stress ◽  
Strand Break ◽  
Upstream Region ◽  
Yeast Genome ◽  
Regulation Of Transcription ◽  
Dependent Manner

AbstractNoncoding RNAs (ncRNAs) are involved in various biological processes, including gene expression, development, and disease. Here, we identify a novel consensus sequence of a cis-element involved in long ncRNA (lncRNA) transcription and demonstrate that lncRNA transcription from this cis-element activates meiotic recombination via chromatin remodeling. In the fission yeast fbp1 gene, glucose starvation induces a series of promoter-associated lncRNAs, referred to as metabolic-stress-induced lncRNAs (mlonRNAs), which contribute to chromatin remodeling and fbp1 activation. Translocation of the cis-element required for mlonRNA into a well-characterized meiotic recombination hotspot, ade6-M26, further stimulates transcription and meiotic recombination via local chromatin remodeling. The consensus sequence of this cis-element (mlon-box) overlaps with meiotic recombination sites in the fission yeast genome. At one such site, the SPBC24C6.09c upstream region, meiotic double-strand break (DSB) formation is induced in an mlon-box-dependent manner. Therefore, mlonRNA transcription plays a universal role in chromatin remodeling and the regulation of transcription and recombination.

The role of RAP1 in the regulation of the MAT alpha locus

1991 ◽  
Vol 11 (2) ◽  
pp. 1069-1079
Author(s):  
D Giesman ◽  
L Best ◽  
K Tatchell
Keyword(s):  
Transcriptional Activation ◽  
Consensus Sequence ◽  
Point Mutations ◽  
Yeast Cells ◽  
Effective Dosage ◽  
Upstream Region ◽  
Yeast Genome ◽  
Temperature Sensitive ◽  
Lacz Gene

The RAP1 gene of Saccharomyces cerevisiae encodes an abundant DNA-binding protein, also known as GRF1, TBA, or TUF, that binds to many sites in the yeast genome in vitro. These sites define a consensus sequence, [sequence: see text], and deletion analyses of genes that contain this sequence have implicated the involvement of RAP1 in numerous cellular processes, including gene activation and repression. The MAT alpha locus, required for determination of the alpha cell type in yeast cells, contains a RAP1 binding site; this site coincides with the MAT alpha upstream activating sequence (UAS) and is necessary for expression of the two genes encoded by the MAT alpha locus, MAT alpha 1 and MAT alpha 2. We show that the MAT alpha UAS is sufficient to activate transcription from a promoterless gene fusion of the yeast CYC1 upstream region and the lacZ gene. Constructs containing only the MAT alpha UAS generated elevated levels of beta-galactosidase activity which were indistinguishable from those of constructs containing the entire MAT alpha intergenic region. Further, the MAT alpha UAS has an intrinsic polarity of transcriptional activation; transcription of CYC1-lacZ was six- to sevenfold higher when the UAS was oriented in the direction normally associated with MAT alpha 2 transcription. Point mutations in the MAT alpha UAS that reduce MAT alpha expression three- to fivefold resulted in a bi-mating phenotype, while a mutation that reduced MAT alpha expression still further resulted in an a-mating phenotype. We isolated plasmids from a high-copy-number yeast library that suppressed the bi-mating defect of point mutations in the MAT alpha UAS, and the most effective dosage suppressor contained the gene encoding RAP1. A temperature-sensitive rap1 mutant bi-mates at the semipermissive temperature. Double mutants at rap1 and mat alpha mate exclusively as a cells, at all temperatures, and do not express detectable levels of MAT alpha RNA. These data provide evidence that the RAP1 gene product functions at the MAT alpha UAS in vivo.

scholarly journals Chromatin remodeler Fft3 plays a dual role at blocked DNA replication forks

2019 ◽  
Vol 2 (5) ◽  
pp. e201900433 ◽  
Author(s):  
Anissia Ait-Saada ◽  
Olga Khorosjutina ◽  
Jiang Chen ◽  
Karol Kramarz ◽  
Vladimir Maksimov ◽  
...  
Keyword(s):  
Dna Damage ◽  
Dna Replication ◽  
Fission Yeast ◽  
Chromatin Remodeling ◽  
Replication Fork ◽  
Strand Break ◽  
Replication Forks ◽  
Damage Repair ◽  
Single Strand Annealing ◽  
Strand Annealing

Here, we investigate the function of fission yeast Fun30/Smarcad1 family of SNF2 ATPase-dependent chromatin remodeling enzymes in DNA damage repair. There are three Fun30 homologues in fission yeast, Fft1, Fft2, and Fft3. We find that only Fft3 has a function in DNA repair and it is needed for single-strand annealing of an induced double-strand break. Furthermore, we use an inducible replication fork barrier system to show that Fft3 has two distinct roles at blocked DNA replication forks. First, Fft3 is needed for the resection of nascent strands, and second, it is required to restart the blocked forks. The latter function is independent of its ATPase activity.

scholarly journals swi6, a gene required for mating-type switching, prohibits meiotic recombination in the mat2-mat3 "cold spot" of fission yeast.

Genetics ◽  
1991 ◽  
Vol 129 (4) ◽  
pp. 1033-1042
Author(s):  
A J Klar ◽  
M J Bonaduce
Keyword(s):  
Fission Yeast ◽  
Mating Type ◽  
Meiotic Recombination ◽  
Hot Spot ◽  
Strand Break ◽  
Double Strand Break ◽  
Cold Spot ◽  
Additional Result ◽  
Type Locus ◽  
Mating Type Switching

Abstract Mitotic interconversion of the mating-type locus (mat1) of the fission yeast Schizosaccharomyces pombe is initiated by a double-strand break at mat1. The mat2 and mat3 loci act as nonrandom donors of genetic information for mat1 switching such that switches occur primarily (or only) to the opposite mat1 allele. Location of the mat1 "hot spot" for transposition should be contrasted with the "cold spot" of meiotic recombination located within the adjoining mat2-mat3 interval. That is, meiotic interchromosomal recombination in mat2, mat3 and the intervening 15-kilobase region does not occur at all. swi2 and swi6 switching-deficient mutants possess the normal level of double-strand break at mat1, yet they fail to switch efficiently. By testing for meiotic recombination in the cold spot, we found the usual lack of recombination in a swi2 mutant but a significant level of recombination in a swi6 mutant. Therefore, the swi6 gene function is required to keep the donor loci inert for interchromosomal recombination. This finding, combined with the additional result that switching primarily occurs intrachromosomally, suggests that the donor loci are made accessible for switching by folding them onto mat1, thus causing the cold spot of recombination.

scholarly journals The SWI/SNF ATP-Dependent Chromatin Remodeling Complex in Arabidopsis Responds to Environmental Changes in Temperature-Dependent Manner

2020 ◽  
Vol 21 (3) ◽  
pp. 762 ◽  
Author(s):  
Dominika M. Gratkowska-Zmuda ◽  
Szymon Kubala ◽  
Elzbieta Sarnowska ◽  
Pawel Cwiek ◽  
Paulina Oksinska ◽  
...  
Keyword(s):  
Plant Growth ◽  
Chromatin Remodeling ◽  
Target Genes ◽  
Environmental Changes ◽  
Fine Tuning ◽  
Regulation Of Transcription ◽  
Dependent Manner ◽  
Growth Responses ◽  
Nucleosome Remodeling ◽  
The Core

SWI/SNF ATP-dependent chromatin remodeling complexes (CRCs) play important roles in the regulation of transcription, cell cycle, DNA replication, repair, and hormone signaling in eukaryotes. The core of SWI/SNF CRCs composed of a SWI2/SNF2 type ATPase, a SNF5 and two of SWI3 subunits is sufficient for execution of nucleosome remodeling in vitro. The Arabidopsis genome encodes four SWI2/SNF2 ATPases, four SWI3, a single SNF5 and two SWP73 subunits. Genes of the core SWI/SNF components have critical but not fully overlapping roles during plant growth, embryogenesis, and sporophyte development. Here we show that the Arabidopsis swi3c mutant exhibits a phenotypic reversion when grown at lower temperature resulting in partial restoration of its embryo, root development and fertility defects. Our data indicates that the swi3c mutation alters the expression of several genes engaged in low temperature responses. The location of SWI3C-containing SWI/SNF CRCs on the ICE1, MYB15 and CBF1 target genes depends on the temperature conditions, and the swi3c mutation thus also influences the transcription of several cold-responsive (COR) genes. These findings, together with genetic analysis of swi3c/ice1 double mutant and enhanced freezing tolerance of swi3c plants illustrate that SWI/SNF CRCs contribute to fine-tuning of plant growth responses to different temperature regimes.

scholarly journals The role of RAP1 in the regulation of the MAT alpha locus.

1991 ◽  
Vol 11 (2) ◽  
pp. 1069-1079 ◽  
Author(s):  
D Giesman ◽  
L Best ◽  
K Tatchell
Keyword(s):  
Transcriptional Activation ◽  
Consensus Sequence ◽  
Point Mutations ◽  
Yeast Cells ◽  
Effective Dosage ◽  
Upstream Region ◽  
Yeast Genome ◽  
Temperature Sensitive ◽  
Lacz Gene

The RAP1 gene of Saccharomyces cerevisiae encodes an abundant DNA-binding protein, also known as GRF1, TBA, or TUF, that binds to many sites in the yeast genome in vitro. These sites define a consensus sequence, [sequence: see text], and deletion analyses of genes that contain this sequence have implicated the involvement of RAP1 in numerous cellular processes, including gene activation and repression. The MAT alpha locus, required for determination of the alpha cell type in yeast cells, contains a RAP1 binding site; this site coincides with the MAT alpha upstream activating sequence (UAS) and is necessary for expression of the two genes encoded by the MAT alpha locus, MAT alpha 1 and MAT alpha 2. We show that the MAT alpha UAS is sufficient to activate transcription from a promoterless gene fusion of the yeast CYC1 upstream region and the lacZ gene. Constructs containing only the MAT alpha UAS generated elevated levels of beta-galactosidase activity which were indistinguishable from those of constructs containing the entire MAT alpha intergenic region. Further, the MAT alpha UAS has an intrinsic polarity of transcriptional activation; transcription of CYC1-lacZ was six- to sevenfold higher when the UAS was oriented in the direction normally associated with MAT alpha 2 transcription. Point mutations in the MAT alpha UAS that reduce MAT alpha expression three- to fivefold resulted in a bi-mating phenotype, while a mutation that reduced MAT alpha expression still further resulted in an a-mating phenotype. We isolated plasmids from a high-copy-number yeast library that suppressed the bi-mating defect of point mutations in the MAT alpha UAS, and the most effective dosage suppressor contained the gene encoding RAP1. A temperature-sensitive rap1 mutant bi-mates at the semipermissive temperature. Double mutants at rap1 and mat alpha mate exclusively as a cells, at all temperatures, and do not express detectable levels of MAT alpha RNA. These data provide evidence that the RAP1 gene product functions at the MAT alpha UAS in vivo.

scholarly journals Distinct Chromatin Modulators Regulate the Formation of Accessible and Repressive Chromatin at the Fission Yeast Recombination Hotspot ade6-M26

2008 ◽  
Vol 19 (3) ◽  
pp. 1162-1173 ◽  
Author(s):  
Kouji Hirota ◽  
Ken-ichi Mizuno ◽  
Takehiko Shibata ◽  
Kunihiro Ohta
Keyword(s):  
Chromatin Remodeling ◽  
Chromatin Structure ◽  
Meiotic Recombination ◽  
Initiation Site ◽  
Regulation Of Transcription ◽  
Transcriptional Initiation ◽  
Recombination Hotspot ◽  
Repressive Chromatin ◽  
Chromatin Configuration ◽  
Responsive Element

Histone acetyltransferases (HATs) and ATP-dependent chromatin remodeling factors (ADCRs) regulate transcription and recombination via alteration of local chromatin configuration. The ade6-M26 allele of Schizosaccharomyces pombe creates a meiotic recombination hotspot that requires a cAMP-responsive element (CRE)-like sequence M26, the Atf1/Pcr1 heterodimeric ATF/CREB transcription factor, the Gcn5 HAT, and the Snf22 SWI2/SNF2 family ADCR. Chromatin alteration occurs meiotically around M26, leading to the activation of meiotic recombination. We newly report the roles of other chromatin remodeling factors that function positively and negatively in chromatin alteration at M26: two CHD-1 family ADCRs (Hrp1 and Hrp3), a Spt-Ada-Gcn5 acetyltransferase component (Ada2), and a member of Moz-Ybf2/Sas3-Sas2-Tip60 family (Mst2). Ada2, Mst2, and Hrp3 are required for the full activation of chromatin changes around M26 and meiotic recombination. Acetylation of histone H3 around M26 is remarkably reduced in gcn5Δ, ada2Δ and snf22Δ, suggesting cooperative functions of these HAT complexes and Snf22. Conversely, Hrp1, another CHD-1 family ADCR, maintains repressive chromatin configuration at ade6-M26. Interestingly, transcriptional initiation site is shifted to a site around M26 from the original initiation sites, in couple with the histone acetylation and meiotic chromatin alteration induced around 3′ region of M26, suggesting a collaboration between these chromatin modulators and the transcriptional machinery to form accessible chromatin. These HATs and ADCRs are also required for the regulation of transcription and chromatin structure around M26 in response to osmotic stress. Thus, we propose that multiple chromatin modulators regulate chromatin structure reversibly and participate in the regulation of both meiotic recombination and stress-induced transcription around CRE-like sequences.

Counteracting Regulation of Chromatin Remodeling at a Fission Yeast cAMP Responsive Element-Related Recombination Hotspot by Stress-Activated Protein Kinase, cAMP-Dependent Kinase and Meiosis Regulators

Genetics ◽  
2001 ◽  
Vol 159 (4) ◽  
pp. 1467-1478 ◽  
Author(s):  
Ken-ichi Mizuno ◽  
Tomoko Hasemi ◽  
Toshiharu Ubukata ◽  
Takatomi Yamada ◽  
Elisabeth Lehmann ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Fission Yeast ◽  
Chromatin Remodeling ◽  
Meiotic Recombination ◽  
Cellular Differentiation ◽  
Dependent Protein Kinase ◽  
Physiological Factors ◽  
Dependent Protein ◽  
Responsive Element ◽  
Pka Pathway

AbstractIn fission yeast, an ATF/CREB-family transcription factor Atf1-Pcr1 plays important roles in the activation of early meiotic processes via the stress-activated protein kinase (SAPK) and the cAMP-dependent protein kinase (PKA) pathways. In addition, Atf1-Pcr1 binds to a cAMP responsive element (CRE)-like sequence at the site of the ade6-M26 mutation, which results in local enhancement of meiotic recombination and chromatin remodeling. Here we studied the roles of meiosis-inducing signal transduction pathways in M26 chromatin remodeling. Chromatin analysis revealed that persistent activation of PKA in meiosis inhibited M26 chromatin remodeling, suggesting that the PKA pathway represses M26 chromatin remodeling. The SAPK pathway activated M26 chromatin remodeling, since mutants lacking a component of this pathway, the Wis1 or Spc1/Sty1 kinases, had no M26 chromatin remodeling. M26 chromatin remodeling also required the meiosis regulators Mei2 and Mei3 but not the subsequently acting regulators Sme2 and Mei4, suggesting that induction of M26 chromatin remodeling needs meiosis-inducing signals before premeiotic DNA replication. Similar meiotic chromatin remodeling occurred meiotically around natural M26 heptamer sequences. These results demonstrate the coordinated action of genetic and physiological factors required to remodel chromatin in preparation for high levels of meiotic recombination and eukaryotic cellular differentiation.

scholarly journals The Saccharomyces cerevisiae RDN1 Locus Is Sequestered From Interchromosomal Meiotic Ectopic Recombination in a SIR2-Dependent Manner

Genetics ◽  
2000 ◽  
Vol 155 (3) ◽  
pp. 1019-1032
Author(s):  
Edward S Davis ◽  
Brenda K Shafer ◽  
Jeffrey N Strathern
Keyword(s):  
Gene Expression ◽  
Meiotic Recombination ◽  
Rdna Locus ◽  
Yeast Genome ◽  
Dependent Manner ◽  
Ectopic Recombination ◽  
The Poor ◽  
Homology Searching ◽  
Low Rate ◽  
Recombination Gene

Abstract Meiotic ectopic recombination occurs at similar frequencies among many sites in the yeast genome, suggesting that all loci are similarly accessible to homology searching. In contrast, we found that his3 sequences integrated in the RDN1 (rDNA) locus were unusually poor participants in meiotic recombination with his3 sequences at other sites. We show that the low rate of meiotic ectopic recombination resulted from the poor ability of RDN1::his3 to act as a donor sequence. SIR2 partially repressed interchromosomal meiotic ectopic recombination at RDN1, consistent with its role in regulating recombination, gene expression, and retrotransposition within RDN1. We propose that RDN1 is physically sequestered from meiotic homology searching mechanisms.

Metabolic stress regulates genome-wide transcription in a PTEN-dependent manner

2020 ◽  
Vol 29 (16) ◽  
pp. 2736-2745
Author(s):  
Ata Abbas ◽  
Roshan Padmanabhan ◽  
Charis Eng
Keyword(s):  
Transcriptional Regulation ◽  
Rna Polymerase Ii ◽  
Cancer Progression ◽  
Metabolic Stress ◽  
Glucose Deprivation ◽  
Regulation Of Transcription ◽  
Dependent Manner ◽  
Loss Of Function ◽  
Genome Wide

Abstract PTEN is implicated in a wide variety of pathophysiological conditions and traditionally studied in the context of the PIK3–AKT–mTOR axis. Recent studies from our group and others have reported a novel role of PTEN in the regulation of transcription at the genome-wide scale. This emerging role of PTEN on global transcriptional regulation is providing a better understanding of various diseases, including cancer. Because cancer progression is an energy-demanding process and PTEN is known to regulate metabolic processes, we sought to understand the role of PTEN in transcriptional regulation under metabolic stress, a condition often developing in the tumor microenvironment. In the present study, we demonstrate that PTEN modulates genome-wide RNA Polymerase II occupancy in cells undergoing glucose deprivation. The glucose-deprived PTEN null cells were found to continue global gene transcription, which may activate a survival mode. However, cells with constitutive PTEN expression slow transcription, an evolutionary mechanism that may save cellular energy and activate programmed cell death pathways, in the absence of glucose. Interestingly, alternative exon usage by PTEN null cells is increased under metabolic stress in contrast to PTEN-expressing cells. Overall, our study demonstrates distinct mechanisms involved in PTEN-dependent genome-wide transcriptional control under metabolic stress. Our findings provide a new insight in understanding tumor pathology and how PTEN loss of function, whether by genetic or non-genetic mechanisms, can contribute to a favorable transcriptional program employed by tumor cells to escape apoptosis, hence developing more aggressive and metastatic phenotypes.

scholarly journals Regulation of Telomere Structure and Functions by Subunits of the INO80 Chromatin Remodeling Complex

2007 ◽  
Vol 27 (16) ◽  
pp. 5639-5649 ◽  
Author(s):  
Eun Young Yu ◽  
Olga Steinberg-Neifach ◽  
Alain T. Dandjinou ◽  
Frances Kang ◽  
Ashby J. Morrison ◽  
...  
Keyword(s):  
Chromatin Remodeling ◽  
Position Effect ◽  
Strand Break ◽  
Telomere Maintenance ◽  
Regulation Of Transcription ◽  
Chromatin Remodeling Complex ◽  
Dna Double Strand Break ◽  
Preferential Localization ◽  
Chromatin Remodeling Complexes ◽  
Tetratricopeptide Repeat Domain

ABSTRACT ATP-dependent chromatin remodeling complexes have been implicated in the regulation of transcription, replication, and more recently DNA double-strand break repair. Here we report that the Ies3p subunit of the Saccharomyces cerevisiae INO80 chromatin remodeling complex interacts with a conserved tetratricopeptide repeat domain of the telomerase protein Est1p. Deletion of IES3 and some other subunits of the complex induced telomere elongation and altered telomere position effect. In telomerase-negative mutants, loss of Ies3p delayed the emergence of recombinational survivors and stimulated the formation of extrachromosomal telomeric circles in survivors. Deletion of IES3 also resulted in heightened levels of telomere-telomere fusions in telomerase-deficient strains. In addition, a delay in survivor formation was observed in an Arp8p-deficient mutant. Because Arp8p is required for the chromatin remodeling activity of the INO80 complex, the complex may promote recombinational telomere maintenance by altering chromatin structure. Consistent with this notion, we observed preferential localization of multiple subunits of the INO80 complex to telomeres. Our results reveal novel functions for a subunit of the telomerase complex and the INO80 chromatin remodeling complex.

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