63 public questions tagged with this topic.
DNA ligase does not break DNA strands; it joins DNA fragments by forming phosphodiester bonds.
Ref: NCERT Class 12 Biology Chapter 10: Biotechnology and its Applications Biosafety and Overview of Applications
DNA ligase forms phosphodiester bonds between DNA fragments, sealing nicks in the sugar-phosphate backbone.
Ref: NCERT Class 12 Biology Chapter 9: Biotechnology: Principles and Processes Bioreactors and Downstream Processing
DNA ligase forms phosphodiester bonds between DNA fragments, sealing nicks in the sugar-phosphate backbone.
Ref: NCERT Class 12 Biology Chapter 9: Biotechnology: Principles and Processes Bioreactors and Downstream Processing
DNA ligase joins the cut DNA fragments by forming phosphodiester bonds between them.
Ref: NCERT Class 12 Biology Chapter 9: Biotechnology: Principles and Processes Polymerase Chain Reaction - PCR and Applications
DNA ligase is responsible for sealing breaks in the sugar-phosphate backbone of DNA, making it essential in recombinant DNA technology.
Ref: NCERT Class 12 Biology Chapter 9: Biotechnology: Principles and Processes Competent Host and Gene Transfer Methods
Single-strand binding proteins (SSBs) prevent the reannealing of separated DNA strands during replication.
Ref: NCERT Class 12 Biology Chapter 5: Molecular Basis of Inheritance Regulation of Gene Expression - Lac Operon
DNA ligase joins Okazaki fragments by forming phosphodiester bonds between them.
Ref: NCERT Class 12 Biology Chapter 5: Molecular Basis of Inheritance DNA Replication - Semiconservative and Machinery
DNA ligase joins Okazaki fragments on the lagging strand by forming phosphodiester bonds.
Ref: NCERT Class 12 Biology Chapter 5: Molecular Basis of Inheritance DNA Replication - Semiconservative and Machinery
Transcription-coupled nucleotide excision repair is subpathway accelerating removal of bulky helix-distorting lesions that block elongating RNA polymerase. When RNA polymerase II stalls at cyclobutane pyrimidine dimer or 6-4 photoproduct located on transcribed template strand, stalled complex is recognized by CSB and CSA ubiquitin ligase recruiting TFIIH and core excision factors. Repair focused exclusively on template strand because non-transcribed strand lesions do not impede polymerase translocation. This strand-specific prioritization ensures rapidly transcribed essential genes restored preferentially, explaining clinical features of Cockayne syndrome defective in this pathway versus global genome repair.
Ref: Watson Molecular Biology of Gene 7th ed. Chapter 10: TCR repairs template strand lesions; Alberts Ch.5 Transcription-coupled NER
Final sealing of processed DNA ends in classical non-homologous end joining performed by DNA ligase IV, dedicated ligase distinct from replication ligase I and base excision ligase III. Ligase IV forms stable obligate complex with XRCC4 scaffold and accessory factor XLF/Cernunnos plus PAXX, enhancing adenylation and end alignment. After Ku and DNA-PKcs orchestrate end processing, XRCC4-Ligase IV complex catalyzes ATP-dependent phosphodiester bond formation joining broken termini. Patient mutations in LIG4 cause immunodeficiency and radiosensitivity, highlighting essential role in lymphocyte V(D)J recombination and general double-strand break repair pathway completion.
Ref: Lodish Chapter 11: NHEJ ligation by Ligase IV XRCC4 complex; J Biol Chem 2018 Mechanism of Ligase IV end joining
Pathway choice for double-strand break repair depends strongly on cell cycle stage and resection control. In G0 quiescence and G1 gap where sister chromatids absent, extensive 5' resection blocked by 53BP1-RIF1-Shieldin complex and Ku end-binding factor prevents homology search. Therefore non-homologous end joining dominates, initiated by Ku70/Ku80 rapidly capping ends and recruiting DNA-PKcs and ligase IV. In S/G2, CDK phosphorylation activates CtIP enabling resection favoring homologous recombination. Thus NHEJ predominance in G0/G1 reflects availability of template and protective mechanisms limiting homologous recombination when homolog unavailable.
Ref: Berg Biochemistry Chapter 28: DSB repair cell cycle choice; NCBI Bookshelf NHEJ in G1 predominance regulation
Double-strand break is most cytotoxic lesion resolved by two major pathways. Non-homologous end joining rapidly ligates ends but can delete nucleotides. Homology-directed repair, also termed homologous recombination repair or HDR, uses sister chromatid present in late S and G2 phases as faithful template. After resection by MRN complex CtIP, Rad51 catalyzes strand invasion forming D-loop, polymerase delta extends using homologous sequence, Holliday junctions resolved. Because homologous donor retains exact original sequence, repair restores information without errors, essential for maintaining genome stability and enabling precise genome editing applications using donor templates.
Ref: Lodish Molecular Cell Biology 9th ed. Chapter 12: HDR error-free DSB repair; Alberts Ch.5 Homologous recombination precise repair
