Replication stress leads to ssDNA accumulation, which affects the mechanisms influencing cell cycle progression in mycATRΔC-/- cells.

<p>(A) Representative images acquired by a LSM880 Zeiss confocal microscope from Z stack images of mycATRΔC-/- cells (cl8) untreated (NT) or treated with 5 mM of HU for 5 hours. Previously, cells were incubated with 150 µM of IdU for 16 hours for DNA labelling. Cells were fixed with 3% formald...

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محفوظ في:
التفاصيل البيبلوغرافية
المؤلف الرئيسي: Gabriel L. A. da Silva (22676649) (author)
مؤلفون آخرون: Jeziel D. Damasceno (9073663) (author), Jennifer A. Black (14411790) (author), Craig Lapsley (6082646) (author), Richard McCulloch (12918) (author), Luiz R. O. Tosi (9073666) (author)
منشور في: 2025
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author Gabriel L. A. da Silva (22676649)
author2 Jeziel D. Damasceno (9073663)
Jennifer A. Black (14411790)
Craig Lapsley (6082646)
Richard McCulloch (12918)
Luiz R. O. Tosi (9073666)
author2_role author
author
author
author
author
author_facet Gabriel L. A. da Silva (22676649)
Jeziel D. Damasceno (9073663)
Jennifer A. Black (14411790)
Craig Lapsley (6082646)
Richard McCulloch (12918)
Luiz R. O. Tosi (9073666)
author_role author
dc.creator.none.fl_str_mv Gabriel L. A. da Silva (22676649)
Jeziel D. Damasceno (9073663)
Jennifer A. Black (14411790)
Craig Lapsley (6082646)
Richard McCulloch (12918)
Luiz R. O. Tosi (9073666)
dc.date.none.fl_str_mv 2025-11-24T18:33:13Z
dc.identifier.none.fl_str_mv 10.1371/journal.pgen.1011899.g003
dc.relation.none.fl_str_mv https://figshare.com/articles/figure/Replication_stress_leads_to_ssDNA_accumulation_which_affects_the_mechanisms_influencing_cell_cycle_progression_in_mycATR_C-_-_cells_/30697536
dc.rights.none.fl_str_mv CC BY 4.0
info:eu-repo/semantics/openAccess
dc.subject.none.fl_str_mv Biophysics
Biochemistry
Microbiology
Cell Biology
Genetics
Molecular Biology
Developmental Biology
Science Policy
Infectious Diseases
Biological Sciences not elsewhere classified
Physical Sciences not elsewhere classified
major &# 8217
div >< p
data reveals loss
cells possess mechanisms
remarkably plastic genome
cas9 genome editing
like family acts
protein kinase ataxia
atr depends upon
delayed dna replication
stranded dna accumulation
leishmania major </
dna damage kinase
dna damage
genome stability
leishmania </
dna metabolism
dna injuries
atr acts
replication stress
replication impediments
work shows
whose integrity
terminal knockout
smaller chromosomes
protozoan parasite
phosphatidylinositol 3
nuclear localisation
mycatrδc -/-).
mycatr ),
master regulator
larger chromosomes
key role
increased levels
functional relevance
eukaryotic response
deletion results
constantly challenged
atr plays
atr homolog
atr ),
dc.title.none.fl_str_mv Replication stress leads to ssDNA accumulation, which affects the mechanisms influencing cell cycle progression in mycATRΔC-/- cells.
dc.type.none.fl_str_mv Image
Figure
info:eu-repo/semantics/publishedVersion
image
description <p>(A) Representative images acquired by a LSM880 Zeiss confocal microscope from Z stack images of mycATRΔC-/- cells (cl8) untreated (NT) or treated with 5 mM of HU for 5 hours. Previously, cells were incubated with 150 µM of IdU for 16 hours for DNA labelling. Cells were fixed with 3% formaldehyde and stained with α-BrdU (ssDNA, green); genomic DNA was stained using DAPI (gray). Dashed squared delimitated a cell zoomed out. (n) nucleus (k) kinetoplast are indicated. Bar scale = 8 um. (B) Quantification of the ssDNA signal in the nucleus of mycATR and mycATRΔC-/- cells treated or not with 5 mM of HU for 5 hours; Cas9T7 cells without α-BrdU were use as negative control. An area was drawn around 150 nuclei based on DAPI staining and ssDNA signal was measured using ImageJ software (Error bars ± SD; n = 2 experiments, p < 0.05; ** p < 0.005; *** p < 0.001; **** p < 0.0001. Unpaired t-test). (C) mycATR and mycATRΔC-/- cells were left untreated (NT) or treated with 0.5 mM of Hydroxyurea (HU) for 20 hours (Chronic) or treated with 5 mM of Hydroxyurea (HU) for 5 hours (Acute), washed and resuspended in fresh media, and samples collected at 0, 2, 5 hours after chronic treatment and 0, 2, 4 hours after acute treatment. Cells were fixed with methanol and DNA stained with propidium iodate, followed by flow cytometer analysis; the cell cycle profile was created using FlowJo software. (D) Representative images of mycATRΔC-/- (cl1) cells pulsed with 150 µM of EdU for 30 minutes in untreated condition or after 5 hours culturing in fresh media post release from chronic HU treatment. Cells were fixed with 3% formaldehyde and a Click-IT reaction was used to stain cells that had uptaken EdU during the 30 min pulse (red); genomic DNA was stained with DAPI (cyan) and α-tubulin was used to stain the cytoskeleton (gray). Dashed squared delimitated a cell zoomed out. (n) nucleus (k) kinetoplast are indicated. Bar = 6 um. (E) Percentage of EdU positive mycATR or mycATRΔC-/- cells in each condition (untreated, after release from chronic (post 5 hours), or acute (post 4 hours) HU treatment) was calculated by the number of positive EdU stained cells divided by the total number of cells present in each sample (100 – 300 cells; error bars ± SD; n = 2 experiments, * p < 0.05; ** p < 0.005; *** p < 0.001; **** p < 0.0001. Unpaired t-test).</p>
eu_rights_str_mv openAccess
id Manara_a736a7c556eca71d418b189fd950c0e0
identifier_str_mv 10.1371/journal.pgen.1011899.g003
network_acronym_str Manara
network_name_str ManaraRepo
oai_identifier_str oai:figshare.com:article/30697536
publishDate 2025
repository.mail.fl_str_mv
repository.name.fl_str_mv
repository_id_str
rights_invalid_str_mv CC BY 4.0
spelling Replication stress leads to ssDNA accumulation, which affects the mechanisms influencing cell cycle progression in mycATRΔC-/- cells.Gabriel L. A. da Silva (22676649)Jeziel D. Damasceno (9073663)Jennifer A. Black (14411790)Craig Lapsley (6082646)Richard McCulloch (12918)Luiz R. O. Tosi (9073666)BiophysicsBiochemistryMicrobiologyCell BiologyGeneticsMolecular BiologyDevelopmental BiologyScience PolicyInfectious DiseasesBiological Sciences not elsewhere classifiedPhysical Sciences not elsewhere classifiedmajor &# 8217div >< pdata reveals losscells possess mechanismsremarkably plastic genomecas9 genome editinglike family actsprotein kinase ataxiaatr depends upondelayed dna replicationstranded dna accumulationleishmania major </dna damage kinasedna damagegenome stabilityleishmania </dna metabolismdna injuriesatr actsreplication stressreplication impedimentswork showswhose integrityterminal knockoutsmaller chromosomesprotozoan parasitephosphatidylinositol 3nuclear localisationmycatrδc -/-).mycatr ),master regulatorlarger chromosomeskey roleincreased levelsfunctional relevanceeukaryotic responsedeletion resultsconstantly challengedatr playsatr homologatr ),<p>(A) Representative images acquired by a LSM880 Zeiss confocal microscope from Z stack images of mycATRΔC-/- cells (cl8) untreated (NT) or treated with 5 mM of HU for 5 hours. Previously, cells were incubated with 150 µM of IdU for 16 hours for DNA labelling. Cells were fixed with 3% formaldehyde and stained with α-BrdU (ssDNA, green); genomic DNA was stained using DAPI (gray). Dashed squared delimitated a cell zoomed out. (n) nucleus (k) kinetoplast are indicated. Bar scale = 8 um. (B) Quantification of the ssDNA signal in the nucleus of mycATR and mycATRΔC-/- cells treated or not with 5 mM of HU for 5 hours; Cas9T7 cells without α-BrdU were use as negative control. An area was drawn around 150 nuclei based on DAPI staining and ssDNA signal was measured using ImageJ software (Error bars ± SD; n = 2 experiments, p < 0.05; ** p < 0.005; *** p < 0.001; **** p < 0.0001. Unpaired t-test). (C) mycATR and mycATRΔC-/- cells were left untreated (NT) or treated with 0.5 mM of Hydroxyurea (HU) for 20 hours (Chronic) or treated with 5 mM of Hydroxyurea (HU) for 5 hours (Acute), washed and resuspended in fresh media, and samples collected at 0, 2, 5 hours after chronic treatment and 0, 2, 4 hours after acute treatment. Cells were fixed with methanol and DNA stained with propidium iodate, followed by flow cytometer analysis; the cell cycle profile was created using FlowJo software. (D) Representative images of mycATRΔC-/- (cl1) cells pulsed with 150 µM of EdU for 30 minutes in untreated condition or after 5 hours culturing in fresh media post release from chronic HU treatment. Cells were fixed with 3% formaldehyde and a Click-IT reaction was used to stain cells that had uptaken EdU during the 30 min pulse (red); genomic DNA was stained with DAPI (cyan) and α-tubulin was used to stain the cytoskeleton (gray). Dashed squared delimitated a cell zoomed out. (n) nucleus (k) kinetoplast are indicated. Bar = 6 um. (E) Percentage of EdU positive mycATR or mycATRΔC-/- cells in each condition (untreated, after release from chronic (post 5 hours), or acute (post 4 hours) HU treatment) was calculated by the number of positive EdU stained cells divided by the total number of cells present in each sample (100 – 300 cells; error bars ± SD; n = 2 experiments, * p < 0.05; ** p < 0.005; *** p < 0.001; **** p < 0.0001. Unpaired t-test).</p>2025-11-24T18:33:13ZImageFigureinfo:eu-repo/semantics/publishedVersionimage10.1371/journal.pgen.1011899.g003https://figshare.com/articles/figure/Replication_stress_leads_to_ssDNA_accumulation_which_affects_the_mechanisms_influencing_cell_cycle_progression_in_mycATR_C-_-_cells_/30697536CC BY 4.0info:eu-repo/semantics/openAccessoai:figshare.com:article/306975362025-11-24T18:33:13Z
spellingShingle Replication stress leads to ssDNA accumulation, which affects the mechanisms influencing cell cycle progression in mycATRΔC-/- cells.
Gabriel L. A. da Silva (22676649)
Biophysics
Biochemistry
Microbiology
Cell Biology
Genetics
Molecular Biology
Developmental Biology
Science Policy
Infectious Diseases
Biological Sciences not elsewhere classified
Physical Sciences not elsewhere classified
major &# 8217
div >< p
data reveals loss
cells possess mechanisms
remarkably plastic genome
cas9 genome editing
like family acts
protein kinase ataxia
atr depends upon
delayed dna replication
stranded dna accumulation
leishmania major </
dna damage kinase
dna damage
genome stability
leishmania </
dna metabolism
dna injuries
atr acts
replication stress
replication impediments
work shows
whose integrity
terminal knockout
smaller chromosomes
protozoan parasite
phosphatidylinositol 3
nuclear localisation
mycatrδc -/-).
mycatr ),
master regulator
larger chromosomes
key role
increased levels
functional relevance
eukaryotic response
deletion results
constantly challenged
atr plays
atr homolog
atr ),
status_str publishedVersion
title Replication stress leads to ssDNA accumulation, which affects the mechanisms influencing cell cycle progression in mycATRΔC-/- cells.
title_full Replication stress leads to ssDNA accumulation, which affects the mechanisms influencing cell cycle progression in mycATRΔC-/- cells.
title_fullStr Replication stress leads to ssDNA accumulation, which affects the mechanisms influencing cell cycle progression in mycATRΔC-/- cells.
title_full_unstemmed Replication stress leads to ssDNA accumulation, which affects the mechanisms influencing cell cycle progression in mycATRΔC-/- cells.
title_short Replication stress leads to ssDNA accumulation, which affects the mechanisms influencing cell cycle progression in mycATRΔC-/- cells.
title_sort Replication stress leads to ssDNA accumulation, which affects the mechanisms influencing cell cycle progression in mycATRΔC-/- cells.
topic Biophysics
Biochemistry
Microbiology
Cell Biology
Genetics
Molecular Biology
Developmental Biology
Science Policy
Infectious Diseases
Biological Sciences not elsewhere classified
Physical Sciences not elsewhere classified
major &# 8217
div >< p
data reveals loss
cells possess mechanisms
remarkably plastic genome
cas9 genome editing
like family acts
protein kinase ataxia
atr depends upon
delayed dna replication
stranded dna accumulation
leishmania major </
dna damage kinase
dna damage
genome stability
leishmania </
dna metabolism
dna injuries
atr acts
replication stress
replication impediments
work shows
whose integrity
terminal knockout
smaller chromosomes
protozoan parasite
phosphatidylinositol 3
nuclear localisation
mycatrδc -/-).
mycatr ),
master regulator
larger chromosomes
key role
increased levels
functional relevance
eukaryotic response
deletion results
constantly challenged
atr plays
atr homolog
atr ),