Chromatin Ubiquitination Guides DNA Double Strand Break Signaling and Repair

Kolobynina, Ksenia; Rapp, Alexander; Cardoso, M. Cristina

doi:10.3389/fcell.2022.928113

Cited by 6 publications

(5 citation statements)

References 359 publications

(331 reference statements)

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“…Ubiquitination serves a crucial role not only in protein degradation but also in various other biological processes, including DNA repair, activation of protein kinases, and transcription [179][180][181][182][183][184]. Additionally, ubiquitination has been implicated in CI and mechanotransduction [87].…”

Section: Ubiquitination: a Key Mechanism In The Pathways Of Cip And D...mentioning

confidence: 99%

The Role of Mechanotransduction in Contact Inhibition of Locomotion and Proliferation

Nakamura

2024

IJMS

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Contact inhibition (CI) represents a crucial tumor-suppressive mechanism responsible for controlling the unbridled growth of cells, thus preventing the formation of cancerous tissues. CI can be further categorized into two distinct yet interrelated components: CI of locomotion (CIL) and CI of proliferation (CIP). These two components of CI have historically been viewed as separate processes, but emerging research suggests that they may be regulated by both distinct and shared pathways. Specifically, recent studies have indicated that both CIP and CIL utilize mechanotransduction pathways, a process that involves cells sensing and responding to mechanical forces. This review article describes the role of mechanotransduction in CI, shedding light on how mechanical forces regulate CIL and CIP. Emphasis is placed on filamin A (FLNA)-mediated mechanotransduction, elucidating how FLNA senses mechanical forces and translates them into crucial biochemical signals that regulate cell locomotion and proliferation. In addition to FLNA, trans-acting factors (TAFs), which are proteins or regulatory RNAs capable of directly or indirectly binding to specific DNA sequences in distant genes to regulate gene expression, emerge as sensitive players in both the mechanotransduction and signaling pathways of CI. This article presents methods for identifying these TAF proteins and profiling the associated changes in chromatin structure, offering valuable insights into CI and other biological functions mediated by mechanotransduction. Finally, it addresses unanswered research questions in these fields and delineates their possible future directions.

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Section: Ubiquitination: a Key Mechanism In The Pathways Of Cip And D...mentioning

confidence: 99%

The Role of Mechanotransduction in Contact Inhibition of Locomotion and Proliferation

Nakamura

2024

IJMS

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“…Ubiquitination serves a crucial role not only in protein degradation but also in various other biological processes, including DNA repair, activation of protein kinases, and transcription [166][167][168][169][170][171]. Additionally, ubiquitination has been implicated in CI and mechanotransduction [81].…”

Section: Ubiquitination In CI and Mechanotransductionmentioning

confidence: 99%

Contact Inhibition and Mechanotransduction

Nakamura

2023

Preprint

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Contact inhibition (CI) represents a crucial tumor-suppressive mechanism responsible for controlling the unbridled growth of cells, thus preventing the formation of cancerous tissues. CI can be further categorized into two distinct yet interrelated components: CI of locomotion (CIL) and CI of proliferation (CIP). These two components of CI have historically been viewed as separate processes, but emerging research indicates that they share both distinctive and common pathways. Moreover, they exhibit intriguing intersections with mechanotransduction, a process that involves cells sensing and responding to mechanical forces. This review article describes the intricate interplay between mechanical forces and CI, shedding light on how these forces regulate CIL and CIP. Emphasis is placed on filamin A (FLNA)-mediated mechanotransduction, elucidating how FLNA senses mechanical forces and translates them into crucial biochemical signals that regulate cell locomotion and proliferation. In addition to FLNA, trans-acting factors (TAFs) emerge as sensitive players in both CI and the mechanotransduction process. This article presents methods for identifying these TAFs and profiling the associated changes in chromatin structure, offering valuable insights into CI and mechanotransduction regulation. Finally, it addresses unanswered research questions in these fields and delineates their possible future directions.

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“…Following DNA damage, RNF8 mediates the ubiquitination and degradation of POLD4/p12, a subunit of DNA polymerase delta. In the absence of POLD4, the DNA polymerase delta complex exhibits higher proofreading activity [9,[31][32][33][34][35]. We used two GFP-tagged proteins as biological indicators to illustrate our ability to micro-irradiate and analyze cell nucleus responses in real-time.…”

Section: Introductionmentioning

confidence: 99%

Recruitment Kinetics of XRCC1 and RNF8 Following MeV Proton and α-Particle Micro-Irradiation

Muggiolu

Torfeh

Simón

et al. 2023

Biology

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Time-lapse fluorescence imaging coupled to micro-irradiation devices provides information on the kinetics of DNA repair protein accumulation, from a few seconds to several minutes after irradiation. Charged-particle microbeams are valuable tools for such studies since they provide a way to selectively irradiate micrometric areas within a cell nucleus, control the dose and the micro-dosimetric quantities by means of advanced detection systems and Monte Carlo simulations and monitor the early cell response by means of beamline microscopy. We used the charged-particle microbeam installed at the AIFIRA facility to perform micro-irradiation experiments and measure the recruitment kinetics of two proteins involved in DNA signaling and repair pathways following exposure to protons and α-particles. We developed and validated image acquisition and processing methods to enable a systematic study of the recruitment kinetics of GFP-XRCC1 and GFP-RNF8. We show that XRCC1 is recruited to DNA damage sites a few seconds after irradiation as a function of the total deposited energy and quite independently of the particle LET. RNF8 is recruited to DNA damage sites a few minutes after irradiation and its recruitment kinetics depends on the particle LET.

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Chromatin Ubiquitination Guides DNA Double Strand Break Signaling and Repair

Cited by 6 publications

References 359 publications

The Role of Mechanotransduction in Contact Inhibition of Locomotion and Proliferation

The Role of Mechanotransduction in Contact Inhibition of Locomotion and Proliferation

Contact Inhibition and Mechanotransduction

Recruitment Kinetics of XRCC1 and RNF8 Following MeV Proton and α-Particle Micro-Irradiation

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