Drosophila Psf2 has a role in chromosome condensation

Chmielewski, Jeffrey P.; Henderson, Laura; Smith, Charlotte M.; Christensen, Tim W.

doi:10.1007/s00412-012-0383-8

Cited by 5 publications

(2 citation statements)

References 39 publications

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“…GINS is a ring-like protein complex that involves PSF1, PSF2 (GINS2), PSF3 and SLD5 and is initially extracted from budding yeast ( 34 ). GINS2 acts as an important subunit of GINS complexes and mediates the initiation of DNA replication in eukaryotic cells ( 35 , 36 ). Previous studies have revealed that GINS2 is associated with the malignancy of some cancer types and is highly expressed in several malignant tumors ( 6 , 12 ), including TC ( 9 ).…”

Section: Discussionmentioning

confidence: 99%

GINS2 affects cell proliferation, apoptosis, migration and invasion in thyroid cancer via regulating MAPK signaling pathway

Zhang

et al. 2021

Mol Med Rep

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Globally, thyroid cancer (TC) is considered to be the commonest endocrine malignancy. GINS complex subunit 2 (GINS2) belongs to the GINS complex family and is associated with cellular migration, invasion and growth. The present study aimed to investigate the underlying mechanisms of GINS2 on cell viability, migration and invasion in TC cells. By using MTT, wound healing and Transwell assays, the cell viability, migration and invasion were determined. Apoptosis was examined by immunofluorescence. Western blotting was used to detect protein expression levels. In the present study, biological function analysis demonstrated that GINS2 interference attenuated cell viability, migration and invasion in TC cell lines (K1 and SW579). It was discovered that, compared with the control group, GINS2 silencing induced apoptosis in TC cells. Additionally, GINS2 interference inhibited key proteins in the MAPK signaling pathway, including JNK, ERK and p38. According to these comparative experiments, GINS2 was considered to act a pivotal part in cell viability, migration and invasion of TC by regulating the MAPK signaling pathway and might be a potential therapeutic target for treating TC.

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Section: Discussionmentioning

confidence: 99%

GINS2 affects cell proliferation, apoptosis, migration and invasion in thyroid cancer via regulating MAPK signaling pathway

Zhang

et al. 2021

Mol Med Rep

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“…Loss of function of the GINS orthologues sld5 and psf1-1 in budding yeast causes growth defects (Takayama et al, 2003) and in Drosophila, impairment of GINS components causes chromosome condensation and genomic integrity defects (Chmielewski et al, 2012;Gouge and Christensen, 2010). Mouse embryos homozygous for mutations in Sld5 and Psf1 die around implantation stages (Mohri et al, 2013;Ueno et al, 2005) whereas in Xenopus, knockdown of psf2 (the frog ortholog of GINS2) results in retinal development defects (Walter et al, 2008).…”

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confidence: 99%

The GINS complex is required for the survival of rapidly proliferating retinal and tectal progenitor cells during zebrafish development

Varga

Csályi

Bertyák

et al. 2020

Preprint

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Efficient and accurate DNA replication is particularly critical in stem and progenitor cells for successful proliferation and survival. The replisome, an amalgam of protein complexes, is responsible for binding potential origins of replication, unwinding the double helix, and then synthesizing complimentary strands of DNA. According to current models, the initial steps of DNA unwinding and opening are facilitated by the CMG complex, which is composed of a GINS heterotetramer that connects Cdc45 with the mini-chromosome maintenance (Mcm) helicase. In this work, we provide evidence that in the absence of GINS function DNA replication is cell autonomously impaired, and we also show that gins1 and gins2 mutants exhibit elevated levels of apoptosis restricted to actively proliferating regions of the central nervous system (CNS). Intriguingly, our results also suggest that the rapid cell cycles during early embryonic development in zebrafish may not require the function of the GINS complex as neither Gins1 nor Gins2 seem to be present during these stages.

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Chl1 DNA helicase and Scc2 function in chromosome condensation through cohesin deposition

Shen

Skibbens

2017

PLoS ONE

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Chl1 DNA helicase promotes sister chromatid cohesion and associates with both the cohesion establishment acetyltransferase Eco1/Ctf7 and the DNA polymerase processivity factor PCNA that supports Eco1/Ctf7 function. Mutation in CHL1 results in precocious sister chromatid separation and cell aneuploidy, defects that arise through reduced levels of chromatin-bound cohesins which normally tether together sister chromatids (trans tethering). Mutation of Chl1 family members (BACH1/BRIP/FANCJ and DDX11/ChlR1) also exhibit genotoxic sensitivities, consistent with a role for Chl1 in trans tethering which is required for efficient DNA repair. Chl1 promotes the recruitment of Scc2 to DNA which is required for cohesin deposition onto DNA. There is limited evidence, however, that Scc2 also directs the deposition onto DNA of condensins which promote tethering in cis (intramolecular DNA links). Here, we test the ability of Chl1 to promote cis tethering and the role of both Chl1 and Scc2 to promote condensin recruitment to DNA. The results reveal that chl1 mutant cells exhibit significant condensation defects both within the rDNA locus and genome-wide. Importantly, chl1 mutant cell condensation defects do not result from reduced chromatin binding of condensin, but instead through reduced chromatin binding of cohesin. We tested scc2-4 mutant cells and similarly found no evidence of reduced condensin recruitment to chromatin. Consistent with a role for Scc2 specifically in cohesin deposition, scc2-4 mutant cell condensation defects are irreversible. We thus term Chl1 a novel regulator of both chromatin condensation and sister chromatid cohesion through cohesin-based mechanisms. These results reveal an exciting interface between DNA structure and the highly conserved cohesin complex.

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Drosophila Psf2 has a role in chromosome condensation

Cited by 5 publications

References 39 publications

GINS2 affects cell proliferation, apoptosis, migration and invasion in thyroid cancer via regulating MAPK signaling pathway

GINS2 affects cell proliferation, apoptosis, migration and invasion in thyroid cancer via regulating MAPK signaling pathway

The GINS complex is required for the survival of rapidly proliferating retinal and tectal progenitor cells during zebrafish development

Chl1 DNA helicase and Scc2 function in chromosome condensation through cohesin deposition

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