 Show Helicases are enzymes that bind and may even remodel nucleic acid or nucleic acid protein complexes. There are DNA and RNA helicases. DNA helicases are essential during DNA replication because they separate double-stranded DNA into single strands allowing each strand to be copied. During DNA
replication, DNA helicases unwind DNA at positions called origins where synthesis will be initiated. DNA helicase continues to unwind the DNA forming a structure called the replication fork, which is named for the forked appearance of the two strands of DNA as they are unzipped apart. The process of breaking the hydrogen bonds between the nucleotide base pairs in double-stranded DNA requires energy. To break the bonds, helicases use the energy stored in a molecule called ATP, which serves as the
energy currency of cells. DNA helicases also function in other cellular processes where double-stranded DNA must be separated, including DNA repair and transcription. RNA helicases are involved in shaping the form of RNA molecules, during all processes involving RNA, such as transcription, splicing, and translation. Further Exploration Concept Links for further exploration
Review DNA helicases, genomic instability, and human genetic diseaseA J van Brabant et al. Annu Rev Genomics Hum Genet. 2000. AbstractDNA helicases are a highly conserved group of enzymes that unwind DNA. They function in all processes in which access to single-stranded DNA is required, including DNA replication, DNA repair and recombination, and transcription of RNA. Defects in helicases functioning in one or more of these processes can result in characteristic human genetic disorders in which genomic instability and predisposition to cancer are common features. So far, different helicase genes have been found mutated in six such disorders. Mutations in XPB and XPD can result in xeroderma pigmentosum, Cockayne syndrome, or trichothiodystrophy. Mutations in the RecQ-like genes BLM, WRN, and RECQL4 can result in Bloom syndrome, Werner syndrome, and Rothmund-Thomson syndrome, respectively. Because XPB and XPD function in both nucleotide excision repair and transcription initiation, the cellular phenotypes associated with a deficiency of each one of them include failure to repair mutagenic DNA lesions and defects in the recovery of RNA transcription after UV irradiation. The functions of the RecQ-like genes are unknown; however, a growing body of evidence points to a function in restarting DNA replication after the replication fork has become stalled. The genomic instability associated with mutations in the RecQ-like genes includes spontaneous chromosome instability and elevated mutation rates. Mouse models for nearly all of these entities have been developed, and these should help explain the widely different clinical features that are associated with helicase mutations. Similar articles
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What is the role of DNA helicase in the replication of DNA
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