Role of Dot1L and H3K79 methylation in regulating somatic hypermutation of immunoglobulin genes | Zendy

Zhi Duan | Zendy; Linda B. Baughn | Zendy; Xiao Hua Wang | Zendy; Yongwei Zhang | Zendy; Varun Gupta | Zendy; Thomas MacCarthy | Zendy; Matthew D. Scharff | Zendy; Guojun Yu | Zendy

AI Assistant Blog Pricing

Home ZAIA Blog

Open Access

Role of Dot1L and H3K79 methylation in regulating somatic hypermutation of immunoglobulin genes

Author(s) -

Zhi Duan,

Linda B. Baughn,

Xiao Hua Wang,

Yongwei Zhang,

Varun Gupta,

Thomas MacCarthy,

Matthew D. Scharff,

Guojun Yu

Publication year - 2021

Publication title -

proceedings of the national academy of sciences

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 5.011

H-Index - 771

eISSN - 1091-6490

pISSN - 0027-8424

DOI - 10.1073/pnas.2104013118

Subject(s) - somatic hypermutation , cytidine deaminase , gene , biology , genetics , transcription (linguistics) , dna , antibody , transcription factor , microbiology and biotechnology , b cell , linguistics , philosophy

Significance The somatic hypermutation of immunoglobulin (Ig) genes is usually required to make antibodies that protect us from foreign and toxic substances. This mutational process is mediated by activation-induced deaminase (AID) and is targeted to the variable (V) part of the Ig genes that encode the antigen-binding site of antibody molecules, leading to higher affinity and more effective antibodies. AID acts on single-stranded DNA that is created during the transcription of the V region. Here, we show that multiple factors that are involved in the release, from pausing to elongation of transcription, contribute to the hypermutation process, supporting the likelihood that transcriptional pausing and elongation make V region single-stranded DNA available to AID-induced mutations.

The content you want is available to Zendy users.

Already have an account? Click here to sign in.

Having issues? You can contact us here

Accelerating Research