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RECON syndrome is a genome instability disorder caused by mutations in the DNA helicase RECQL1.

Authors :
Abu-Libdeh B
Jhujh SS
Dhar S
Sommers JA
Datta A
Longo GM
Grange LJ
Reynolds JJ
Cooke SL
McNee GS
Hollingworth R
Woodward BL
Ganesh AN
Smerdon SJ
Nicolae CM
Durlacher-Betzer K
Molho-Pessach V
Abu-Libdeh A
Meiner V
Moldovan GL
Roukos V
Harel T
Brosh RM Jr
Stewart GS
Source :
The Journal of clinical investigation [J Clin Invest] 2022 Mar 01; Vol. 132 (5).
Publication Year :
2022

Abstract

Despite being the first homolog of the bacterial RecQ helicase to be identified in humans, the function of RECQL1 remains poorly characterized. Furthermore, unlike other members of the human RECQ family of helicases, mutations in RECQL1 have not been associated with a genetic disease. Here, we identify 2 families with a genome instability disorder that we have named RECON (RECql ONe) syndrome, caused by biallelic mutations in the RECQL gene. The affected individuals had short stature, progeroid facial features, a hypoplastic nose, xeroderma, and skin photosensitivity and were homozygous for the same missense mutation in RECQL1 (p.Ala459Ser), located within its zinc binding domain. Biochemical analysis of the mutant RECQL1 protein revealed that the p.A459S missense mutation compromised its ATPase, helicase, and fork restoration activity, while its capacity to promote single-strand DNA annealing was largely unaffected. At the cellular level, this mutation in RECQL1 gave rise to a defect in the ability to repair DNA damage induced by exposure to topoisomerase poisons and a failure of DNA replication to progress efficiently in the presence of abortive topoisomerase lesions. Taken together, RECQL1 is the fourth member of the RecQ family of helicases to be associated with a human genome instability disorder.

Details

Language :
English
ISSN :
1558-8238
Volume :
132
Issue :
5
Database :
MEDLINE
Journal :
The Journal of clinical investigation
Publication Type :
Academic Journal
Accession number :
35025765
Full Text :
https://doi.org/10.1172/JCI147301