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Section: Genetics » Chemistry of the Gene » Synthesis, Modification and Repair of DNA
 
 
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  DNA repair and genetic diseases in humans
 
     
 
Content
⇒ Chemistry of the Gene 2.  Synthesis, Modification and Repair of DNA
⇒ DNA replication: general features 
⇒ Semi-conservative DNA replication in E. coli
⇒ Semi-conservative replication of chromosomes in eukaryotes
⇒ Semi-discontinuous DNA replication
⇒ Unidirectional and bidirectional DNA replication
⇒ RNA primers in DNA replication
⇒ Regulation of DNA replication by anti-sense RNA primer
⇒ Prokaryotic DNA polymerases
⇒ Eukaryotic DNA polymerases
⇒ Replicons for DNA replication
⇒ DNA replication in prokaryotes 
⇒ Experimental approaches for the study of DNA replication
⇒ Initiation of DNA replication
⇒ Elongation of DNA chain
⇒ Replication fork movement
⇒ Termination of DNA replication
⇒ DNA replication in eukaryotes 
⇒ DNA replication and cell cycle
⇒ Replication origins and initiation of DNA replication (cis and trans-acting elements)
⇒ Comparison of initiation of DNA replication with transcription initiation
⇒ Different steps involved in eukaryotic DNA replication
⇒ Synthesis of telomeric DNA by telomerase
⇒ Models of DNA replication
⇒ Replication fork model
⇒ Rolling circle model of DNA replication
⇒ Mitochondrial DNA replication and D-loops
⇒ RNA directed DNA synthesis (reverse transcription)
⇒ DNA modification and DNA restriction
⇒ DNA repair
⇒ Excision repair systems in E. coli
⇒ An SOS repair system in E. coli
⇒ DNA repair and genetic diseases in humans
DNA repair and genetic diseases in humans
Several genetic diseases in human beings are characterized by cellular hypersensitivity to DNA damage. These diseases also cause increased risk of cancer. Four such recessively inherited diseases include the following : (i) Fanconi anaemia (FA); (ii) Xeroderma pigmentosum (XP); (iii) Ataxia telangiectasia (AT) and (iv) Bloom's syndrome (BS); cells from patients with the first three diseases are uniquely sensitive to DNA damage by DNA cross-linking agents, ultraviolet light and ionizing radiations respectively, those with BS are moderately hypersensitive to several agents causing different types of DNA damage. Genes responsible for two of these diseases (FA, XP) have been identified recently by complementation of hypersensitive cell lines using DNA expression cloning technology (see Genetic Engineering and Biotechnology 1.  Recombinant DNA and PCR (Cloning and Amplification of DNA) for cloning). The XP DNA products show significant similarity to the products of the RAD DNA repair gene of budding yeast, and ERCC genes of rodents (Table 26.7), which are involved in the nucleotide excision repair showing that the essential enzymes involved in DNA metabolism have been conserved through evolution. In future more work on the molecular mechanism of these diseases involving DNA damage will be done.

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*XPAC (and so on) is the term for the gene encoding a protein that corrects XP-A.
+ Rodent complementation groups are numbered. The human genes correcting the defect of rodent mutants are designated ERCC (for excision repair cross complementing) genes, the number referring to the number of the corrected group.
++ Level and type of homology not conclusive.

 
     






     
     
 
 
     
 
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