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Metabolic Modifications in Genomic Stability Maintenance

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A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (31 March 2023) | Viewed by 11581

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Special Issue Editors

Prof. Dr. Xingzhi Xu

E-Mail Website
Guest Editor

College of Medicine, Shenzhen University, Shenzhen, China
Interests: DNA damage response; DNA double strand break; DNA replication; post-translational modifications; ubiquitination; UFMylation

Prof. Dr. Shunichi Takeda

E-Mail Website
Co-Guest Editor

College of Medicine, Shenzhen University, Shenzhen, China
Interests: DNA repair; DNA recombination; gene therapy; chemotherapy of cancer; radiation biology

Special Issue Information

Dear Colleagues,

Active and proper metabolism is essential for cell growth and proliferation. Metabolic reprograming drives tumorigenesis that is enabled by genome instability, among other things. Both normal and abnormal metabolism generate metabolites, which are substrates for post-translation protein modifications. These metabolic modifications include acetylation, methylation, ADP-ribosylation, glycosylation, palmitoylation, malonylation, succinylation, hydroxybutyrylation, crotonylation, and lactylation and play important roles in the maintenance of genome stability. This Special Issue will focus on (1) the identification and characterization of writers, readers, and erasers of newly identified metabolic modifications; (2) the function and mechanism of metabolic modifications in regulating cell cycle progression, DNA replication, the DNA replication stress response, and the DNA damage response; (3) the investigation of metabolic modifications as a potential target for cancer therapy.

Prof. Dr. Xingzhi Xu
Prof. Dr. Shunichi Takeda
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomolecules is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

metabolic modifications
metabolic reprograming
cell cyle
DNA replication
DNA replication stress response
DNA damage response
genome stability

Published Papers (5 papers)

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Research

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23 pages, 7799 KiB

Open AccessArticle

Claspin-Dependent and -Independent Chk1 Activation by a Panel of Biological Stresses

by Hao-Wen Hsiao, Chi-Chun Yang and Hisao Masai

Biomolecules 2023, 13(1), 125; https://doi.org/10.3390/biom13010125 - 7 Jan 2023

Cited by 2 | Viewed by 2127 | Correction

Abstract

Replication stress has been suggested to be an ultimate trigger of carcinogenesis. Oncogenic signal, such as overexpression of CyclinE, has been shown to induce replication stress. Here, we show that various biological stresses, including heat, oxidative stress, osmotic stress, LPS, hypoxia, and arsenate induce activation of Chk1, a key effector kinase for replication checkpoint. Some of these stresses indeed reduce the fork rate, inhibiting DNA replication. Analyses of Chk1 activation in the cell population with Western analyses showed that Chk1 activation by these stresses is largely dependent on Claspin. On the other hand, single cell analyses with Fucci cells indicated that while Chk1 activation during S phase is dependent on Claspin, that in G1 is mostly independent of Claspin. We propose that various biological stresses activate Chk1 either directly by stalling DNA replication fork or by some other mechanism that does not involve replication inhibition. The former pathway predominantly occurs in S phase and depends on Claspin, while the latter pathway, which may occur throughout the cell cycle, is largely independent of Claspin. Our findings provide evidence for novel links between replication stress checkpoint and other biological stresses and point to the presence of replication-independent mechanisms of Chk1 activation in mammalian cells. Full article

(This article belongs to the Special Issue Metabolic Modifications in Genomic Stability Maintenance)

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Review

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27 pages, 2165 KiB

Open AccessReview

Post-Translational Modifications by Lipid Metabolites during the DNA Damage Response and Their Role in Cancer

by Guangrong Zhu, Xiangyang Zheng, Zhifeng Wang and Xingzhi Xu

Biomolecules 2022, 12(11), 1655; https://doi.org/10.3390/biom12111655 - 8 Nov 2022

Viewed by 2298

Abstract

Genomic DNA damage occurs as an inevitable consequence of exposure to harmful exogenous and endogenous agents. Therefore, the effective sensing and repair of DNA damage are essential for maintaining genomic stability and cellular homeostasis. Inappropriate responses to DNA damage can lead to genomic instability and, ultimately, cancer. Protein post-translational modifications (PTMs) are a key regulator of the DNA damage response (DDR), and recent progress in mass spectrometry analysis methods has revealed that a wide range of metabolites can serve as donors for PTMs. In this review, we will summarize how the DDR is regulated by lipid metabolite-associated PTMs, including acetylation, S-succinylation, N-myristoylation, palmitoylation, and crotonylation, and the implications for tumorigenesis. We will also discuss potential novel targets for anti-cancer drug development. Full article

(This article belongs to the Special Issue Metabolic Modifications in Genomic Stability Maintenance)

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12 pages, 1010 KiB

Open AccessReview

Lysine Crotonylation: An Emerging Player in DNA Damage Response

by Yuqin Zhao, Shuailin Hao, Wenchi Wu, Youhang Li, Kaiping Hou, Yu Liu, Wei Cui, Xingzhi Xu and Hailong Wang

Biomolecules 2022, 12(10), 1428; https://doi.org/10.3390/biom12101428 - 5 Oct 2022

Cited by 6 | Viewed by 2437

Abstract

The DNA damage response (DDR) system plays an important role in maintaining genome stability and preventing related diseases. The DDR network comprises many proteins and posttranslational modifications (PTMs) to proteins, which work in a coordinated manner to counteract various genotoxic stresses. Lysine crotonylation (Kcr) is a newly identified PTM occurring in both core histone and non-histone proteins in various organisms. This novel PTM is classified as a reversible acylation modification, which is regulated by a variety of acylases and deacylases and the intracellular crotonyl-CoA substrate concentration. Recent studies suggest that Kcr links cellular metabolism with gene regulation and is involved in numerous cellular processes. In this review, we summarize the regulatory mechanisms of Kcr and its functions in DDR, including its involvement in double-strand break (DSB)-induced transcriptional repression, DSB repair, and the DNA replication stress response. Full article

(This article belongs to the Special Issue Metabolic Modifications in Genomic Stability Maintenance)

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16 pages, 1693 KiB

Open AccessReview

Multifaceted Roles of the N⁶-Methyladenosine RNA Methyltransferase METTL3 in Cancer and Immune Microenvironment

by Chenxi Hu, Jiacheng Liu, Yue Li, Wei Jiang, Ding Ji, Wei Liu and Teng Ma

Biomolecules 2022, 12(8), 1042; https://doi.org/10.3390/biom12081042 - 28 Jul 2022

Cited by 5 | Viewed by 3203

Abstract

As the most abundant internal mRNA modification in eukaryotic cells, N⁶-methyladenosine (m⁶A) has emerged as an important regulator of gene expression and has a profound impact on cancer initiation and progression. mRNA m⁶A modification is regulated by m⁶A methyltransferases, demethylases and reader proteins to fine tune gene expression at the post-transcriptional level. The most well-studied m⁶A methyltransferase, METTL3, plays critical roles in regulating gene expression and affecting the outcome of various cancers. In this review, we discuss the multifaceted roles of METTL3 in regulating specific molecular signaling pathways in different types of cancers and the recent progress on how METTL3 impacts the tumor immune microenvironment. Finally, we discuss future directions and the potential for therapeutic targeting of METTL3 in cancer treatment. Full article

(This article belongs to the Special Issue Metabolic Modifications in Genomic Stability Maintenance)

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