Long interspersed element-1 (LINE-1 or L1) retrotransposons represent the only functional family of autonomous transposable elements in humans and formed 17% of our genome. Even though most of the human L1 sequences are inactive, a limited number of copies per individual retain the ability to mobilize by a process termed retrotransposition. The ongoing L1 retrotransposition may result in insertional mutagenesis that could lead to negative consequences such as genetic disease and cancer. For this reason, cells have evolved several mechanisms of defense to restrict L1 activity. Among them, a critical role for cellular deaminases [activation-induced deaminase (AID)/apolipoprotein B mRNA-editing catalytic polypeptide-like (APOBEC) and adenosine deaminases that act on RNA (ADAR) enzymes] has emerged. The majority of the AID/APOBEC family of proteins are responsible for the deamination of cytosine to uracil (C-to-U editing) within DNA and RNA targets. The ADARs convert adenosine bases to inosines (A-to-I editing) within double-stranded RNA (dsRNA) targets. This review will discuss the current understanding of the regulation of LINE-1 retrotransposition mediated by these enzymes.

Orecchini, E., Frassinelli, L., Galardi, S., Ciafrè, S.a., Michienzi, A. (2018). Post-transcriptional regulation of LINE-1 retrotransposition by AID/APOBEC and ADAR deaminases. CHROMOSOME RESEARCH, 26(1-2), 45-59-59 [10.1007/s10577-018-9572-5].

Post-transcriptional regulation of LINE-1 retrotransposition by AID/APOBEC and ADAR deaminases

Orecchini, Elisa
Membro del Collaboration Group
;
Frassinelli, Loredana
Membro del Collaboration Group
;
Galardi, Silvia
Membro del Collaboration Group
;
Ciafrè, Silvia Anna
Membro del Collaboration Group
;
Michienzi, Alessandro
2018-03-01

Abstract

Long interspersed element-1 (LINE-1 or L1) retrotransposons represent the only functional family of autonomous transposable elements in humans and formed 17% of our genome. Even though most of the human L1 sequences are inactive, a limited number of copies per individual retain the ability to mobilize by a process termed retrotransposition. The ongoing L1 retrotransposition may result in insertional mutagenesis that could lead to negative consequences such as genetic disease and cancer. For this reason, cells have evolved several mechanisms of defense to restrict L1 activity. Among them, a critical role for cellular deaminases [activation-induced deaminase (AID)/apolipoprotein B mRNA-editing catalytic polypeptide-like (APOBEC) and adenosine deaminases that act on RNA (ADAR) enzymes] has emerged. The majority of the AID/APOBEC family of proteins are responsible for the deamination of cytosine to uracil (C-to-U editing) within DNA and RNA targets. The ADARs convert adenosine bases to inosines (A-to-I editing) within double-stranded RNA (dsRNA) targets. This review will discuss the current understanding of the regulation of LINE-1 retrotransposition mediated by these enzymes.
mar-2018
Pubblicato
Rilevanza internazionale
Articolo
Esperti anonimi
Settore BIO/13 - BIOLOGIA APPLICATA
English
ADAR enzymes; AID/APOBEC proteins; Alu; LINE-1; Retrotransposon
Orecchini, E., Frassinelli, L., Galardi, S., Ciafrè, S.a., Michienzi, A. (2018). Post-transcriptional regulation of LINE-1 retrotransposition by AID/APOBEC and ADAR deaminases. CHROMOSOME RESEARCH, 26(1-2), 45-59-59 [10.1007/s10577-018-9572-5].
Orecchini, E; Frassinelli, L; Galardi, S; Ciafrè, Sa; Michienzi, A
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2108/195370
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