Category Archives: helicase

Drosophila CG6539 is orthologue of vertebrate gemin3

Mutations in the survival motor neuron (SMN1) gene cause spinal muscular atrophy (SMA), an autosomal recessive disorder characterised by degeneration of spinal cord motor neurons leading to progressive muscular weakness. SMN1 encodes an RNA-binding protein, SMN, which is complexed with Gemin proteins. Vertebrate Gemin3 is the only RNA helicase in the SMN complex. In Drosophila melanogaster, CG6539 was identified as the orthologue of vertebrate gemin3. It was shown to physically interact with SMN, and its loss results into larval/prepupal lethality. Before death, gemin3 mutant larvae exhibit declined mobility and expanded neuromuscular junctions.

Cauchi RJ, Davies KE, Liu J-L (2008) A Motor Function for the DEAD-Box RNA Helicase, Gemin3, in Drosophila. PLoS Genet 4(11): e1000265. doi:10.1371/journal.pgen.1000265

10.1371/journal.pgen.1000265.g008

doi:10.1371/journal.pgen.1000265.g008

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Filed under biochemistry, biological sciences, biology, cell biology, deletion, drosophila, helicase, lethality, life sciences, science

human exonuclease 1 and BLM helicase

In a recent paper by Amitabh Nimonkar and colleagues, it was established that human BLM helicase, a member of the RecQ family, stimulates human exonuclease 1 (hExo1), a 5′ – 3′ double-stranded DNA exonuclease … “Stimulation of DNA resection by hExo1 is independent of BLM helicase activity and is, instead, mediated by an interaction between the 2 proteins. DNA ends resected by hExo1 and BLM are used by human Rad51, but not its yeast or bacterial counterparts, to promote homologous DNA pairing.”

Nimonkar AV, Oözsoy AZ, Genschel J, Modrich P, Kowalczykowski SC.
Human exonuclease 1 and BLM helicase interact to resect DNA and initiate DNA repair.
Proc Natl Acad Sci U S A. 2008 Oct 29. [Epub ahead of print]

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Filed under biochemistry, biology, DNA, DNA repair, double strand break, exonuclease, genetics, helicase, homologous recombination, molecular biology

WRN mini-review

In a recent issue of DNA Repair [7 (2008) 1776–1786], Julia Sidorova reviews the role of WRN in preserving DNA integrity during replication and propose that WRN can function in coordinating replication fork progression with replication stress-induced fork remodeling. She further discusses damage tolerance pathways, redundancy, and cooperation with other RecQ helicases.


Fig. 3. Possible scenarios of WRN function in coordinating fork progression with damage repair via control over daughter/daughter duplex expansion and/or half-life. (A) An unproductive daughter/daughter duplex with the 3′ overhang is unwound to redirect damage bypass towards translesion synthesis (TLS). (B) An extension of a daughter/daughter duplex leads to exposure of ssDNA regions of mother strands (for simplicity, only one of the strands is shown coated with RPA). Accumulation of RPA stimulates helicase activity of WRN to limit propagation of daughter/daughter duplex and restore an original fork conformation. (C) Lagging strand synthesis in the presence of a daughter/daughter duplex can lead to formation of long flaps. WRN can prevent their formation by limiting half-life of a daughter/daughter duplex, or stimulate FEN-1 to cleave such flaps once they are formed.

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Filed under ageing, aging, biological sciences, biology, DNA, DNA repair, double strand break, exonuclease, genetics, helicase, homologous recombination, lifespan, longevity, molecular biology, nucleus, science, Werner Syndrome, Werners Syndrome, WRN