APOBECs orchestrate genomic and epigenomic editing across health and disease.

  title={APOBECs orchestrate genomic and epigenomic editing across health and disease.},
  author={Karla Cervantes-Gracia and Anna Gramalla-Schmitz and Julian Weischedel and Richard Chahwan},
  journal={Trends in genetics : TIG},
6 Citations

The Methylation Game: Epigenetic and Epitranscriptomic Dynamics of 5-Methylcytosine

This work has revealed extensive crosstalk between epigenetic and epitranscriptomic pathways, adding a new layer of complexity to the understanding of cellular programming and responses to environmental cues.

Distinctive High Expression of Antiretroviral APOBEC3 Protein in Mouse Germinal Center B Cells

To precisely follow the possible activation-induced changes in expression levels of APOBEC3 protein in different mouse tissues and cell populations, genome editing was utilized to establish knock-in mice that express APOBec3 protein with an in-frame FLAG tag.

Expression of Human Endogenous Retroviruses in the Human Thymus Along T Cell Development

A tight regulation of HERV expression during human T cell development is found, with possible implications for the process of T cell selection, as well as the interplay with host restriction factors and potential underlying pathways.

Singularity and Commonality in Response to SARS-CoV-2 in Lung and Colon Cell Models

This study provides gene expression level evidence for the cellular responses attributed to pulmonary and gastrointestinal manifestations of COVID-19 and proposes APOBEC3G as a promising intrinsic antiviral factor of the host response to SARS-CoV-2.

Integrative OMICS Data-Driven Procedure Using a Derivatized Meta-Analysis Approach

A new unifying, scalable and straightforward methodology to meta-analyze different omics outputs, but also to integrate the significant outcomes into novel pathways describing biological processes of interest is described.



Epitranscriptomic profiling across cell types reveals associations between APOBEC1-mediated RNA editing, gene expression outcomes, and cellular function

It is shown that Apolipoprotein B mRNA-editing enzyme, catalytic polypeptide-1 (APOBEC1), together with its cofactor RBM47, mediates robust editing in different tissues and that APOBec1-mediated transcriptome diversification is required for the fine-tuning of protein expression in monocytes, suggesting an epitranscriptomic mechanism for the proper maintenance of homeostasis in innate immune cells.

The Antiviral and Cancer Genomic DNA Deaminase APOBEC3H Is Regulated by an RNA-Mediated Dimerization Mechanism.

The DNA damage induced by the Cytosine Deaminase APOBEC3A Leads to the production of ROS

It is shown that A3A editing of cellular DNA leads to reactive oxygen species (ROS) production through Nox-enzymes, and for the first time, this activity results in the induction of a pro-inflammatory state that may possibly contribute to the constitution of a tumorigenic-prone environment.

Epigenomic Modifications Mediating Antibody Maturation

The combination of histone modifications, DNA methylation status, and non-coding RNAs are assessed and discussed to discuss how they contribute to initiating differential DNA repair pathways at the Ig locus, which ultimately leads to enhanced antibody–antigen binding affinity (SHM) or antibody isotype switching (CSR).

Crosstalk between genetic and epigenetic information through cytosine deamination.

Mitochondrial hypoxic stress induces widespread RNA editing by APOBEC3G in natural killer cells

APOBEC3G is an endogenous RNA editing enzyme in primary natural killer cells and lymphoma cell lines that is induced by cellular crowding and mitochondrial respiratory inhibition to promote adaptation to hypoxic stress.

Activation-induced Cytidine Deaminase Deaminates 5-Methylcytosine in DNA and Is Expressed in Pluripotent Tissues

It is shown that Aid and Apobec1 are 5-methylcytosine deaminases resulting in a thymine base opposite a guanine, which can lead to C → T transition mutations in methylated DNA, or in conjunction with repair of the T:G mismatch, to demethylation.

Endogenous APOBEC3B Overexpression Constitutively Generates DNA Substitutions and Deletions in Myeloma Cells

The results suggest that A3B constitutively mutates the tumour genome beyond the protection of the DNA repair system, which may lead to clonal evolution and genomic instability in myeloma.

LTR retroelement expansion of the human cancer transcriptome and immunopeptidome revealed by de novo transcript assembly.

The current assembly doubled the number of previously annotated transcripts overlapping with long-terminal repeat (LTR) elements, several thousand of which were expressed specifically in one or a few related cancer types.

DNA mismatch repair promotes APOBEC3-mediated diffuse hypermutation in human cancers

A new statistical framework to classify mutagenesis clusters identifies a novel, diffuse hypermutation pattern, named omikli, that is induced by APOBEC3 and associated with mismatch-repair activity, which has a high propensity to generate impactful mutations.