PICH, a Centromere-Associated SNF2 Family ATPase, Is Regulated by Plk1 and Required for the Spindle Checkpoint

Baumann, Christoph; Körner, Roman; Hofmann, Kay; Nigg, Erich A.

doi:10.1016/j.cell.2006.11.041

Cited by 311 publications

(579 citation statements)

References 55 publications

Supporting

Mentioning

521

Contrasting

Unclassified

Order By: Relevance

“…It is recruited to HR-UFBs in early anaphase when the two sister chromatids are just separating [22,23]. PICH is a member of the SNF2 family of DNA-dependent ATPases that possesses dsDNA translocase activity [5]. A key property of PICH is that it displays a high affinity for stretched dsDNA [54].…”

Section: Proteins That Recognize and Process Hr-ufbsmentioning

confidence: 99%

“…Based on these studies, it is conceivable that UFBs arising from unresolved replication/recombination intermediates might also be acted upon by ANKLE1. However, given that UFBs have not been observed in C. elegans embryos and a PICH ortholog has yet to be described for C. elegans [5,66], any involvement of ANKLE1 in the processing of UFBs in higher organisms remains to be determined.…”

Section: A Role Of Lem-3/ankle1 In the Resolution Of Dna Bridges?mentioning

confidence: 99%

“…UFBs, visualized as long fine DNA threads that cannot be detected by conventional DNA staining and are devoid of histones, were previously identified as a special class of mitotic DNA structures that interlink two separating sister chromatids [3,4]. Their discovery came from the immunofluorescent staining of proteins that bind them, including BLM (Bloom’s syndrome helicase), PICH (PLK1-interacting checkpoint helicase) and RPA (replication protein A) [5–8]. …”

Section: Introductionmentioning

confidence: 99%

“…CENP-A, HEC1) at the bridges’ termini. C-UFBs exist in every mitosis and their numbers are increased by treatment with the topoisomerase IIα inhibitor ICRF-193, indicating that they are readily removed by this topoisomerase [5,6,9,10]. Second, DNA catenanes that persist at ribosomal DNA (rDNA) loci give rise to R-UFBs that colocalise with the ribosomal RNA transcription factor UBF, a marker for rDNA [11].…”

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

A new class of ultrafine anaphase bridges generated by homologous recombination

Chan

West

2018

Cell Cycle

View full text Add to dashboard Cite

Ultrafine anaphase bridges (UFBs) are a potential source of genome instability that is a hallmark of cancer. UFBs can arise from DNA catenanes at centromeres/rDNA loci, late replication intermediates induced by replication stress, and DNA linkages at telomeres. Recently, it was reported that DNA intertwinements generated by homologous recombination give rise to a new class of UFBs, which have been termed homologous recombination ultrafine bridges (HR-UFBs). HR-UFBs are decorated with PICH and BLM in anaphase, and are subsequently converted to RPA-coated, single-stranded DNA bridges. Breakage of these sister chromatid entanglements leads to DNA damage that can be repaired by non-homologous end joining in the next cell cycle, but the potential consequences include DNA rearrangements, chromosome translocations and fusions. Visualisation of these HR-UFBs, and knowledge of how they arise, provides a molecular basis to explain how upregulation of homologous recombination or failure to resolve recombination intermediates leads to the development of chromosomal instability observed in certain cancers.

show abstract

Section: Proteins That Recognize and Process Hr-ufbsmentioning

confidence: 99%

Section: A Role Of Lem-3/ankle1 In the Resolution Of Dna Bridges?mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

A new class of ultrafine anaphase bridges generated by homologous recombination

Chan

West

2018

Cell Cycle

View full text Add to dashboard Cite

show abstract

“…First, the PICH helicase has a role in the processing of anaphase bridges [59,60]. Although PICH might not be directly involved in the dissolution of the bridge, it is required to stabilize the DNA and recruit BLM to allow their repair [61].…”

Section: Rs As a Fuel Of Tumorogenesismentioning

confidence: 99%

Replication stress and cancer: It takes two to tango

Lecona

Fernández-Capetillo

2014

Experimental Cell Research

119

107

View full text Add to dashboard Cite

Problems arising during DNA replication require the activation of the ATR-CHK1 pathway to ensure the stabilization and repair of the forks, and to prevent the entry into mitosis with unreplicated genomes. Whereas the pathway is essential at the cellular level, limiting its activity is particularly detrimental for some cancer cells. Here we review the links between replication stress (RS) and cancer, which provide a rationale for the use of ATR and Chk1 inhibitors in chemotherapy. First, we describe how the activation of oncogene-induced RS promotes genome rearrangements and chromosome instability, both of which could potentially fuel carcinogenesis. Next, we review the various pathways that contribute to the suppression of RS, and how mutations in these components lead to increased cancer incidence and/or accelerated ageing. Finally, we summarize the evidence showing that tumours with high levels of RS are dependent on a proficient RS-response, and therefore vulnerable to ATR or Chk1 inhibitors.

show abstract

PICH Supports Embryonic Hematopoiesis by Suppressing a cGAS‐STING‐Mediated Interferon Response

Geng

Zhang

et al. 2022

Advanced Science

View full text Add to dashboard Cite

The Plk1‐interacting checkpoint helicase (PICH) protein localizes to ultrafine anaphase DNA bridges in mitosis along with a complex of DNA repair proteins. Previous studies show PICH deficiency‐induced embryonic lethality in mice. However, the function of PICH that is required to suppress embryonic lethality in PICH‐deficient mammals remains to be determined. Previous clinical studies suggest a link between PICH deficiency and the onset of acquired aplastic anemia. Here, using Pich knock‐out (KO) mouse models, the authors provide evidence for a mechanistic link between PICH deficiency and defective hematopoiesis. Fetal livers from Pich‐KO embryos exhibit a significantly elevated number of hematopoietic stem cells (HSCs); however, these HSCs display a higher level of apoptosis and a much‐reduced ability to reconstitute a functional hematopoietic system when transplanted into lethally irradiated recipients. Moreover, these HSCs show an elevated cytoplasmic dsDNA expression and an activation of the cGAS‐STING pathway, resulting in excessive production of type I interferons (IFN). Importantly, deletion of Ifnar1 or cGAS reverses the defective hematopoiesis. The authors conclude that loss of PICH results in defective hematopoiesis via cGAS‐STING‐mediated type I IFN production.

show abstract

PICH, a Centromere-Associated SNF2 Family ATPase, Is Regulated by Plk1 and Required for the Spindle Checkpoint

Cited by 311 publications

References 55 publications

A new class of ultrafine anaphase bridges generated by homologous recombination

A new class of ultrafine anaphase bridges generated by homologous recombination

Replication stress and cancer: It takes two to tango

PICH Supports Embryonic Hematopoiesis by Suppressing a cGAS‐STING‐Mediated Interferon Response

Contact Info

Product

Resources

About