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Interpretation of NEM inhibition of DNA synthesis insi tu is difticult since, in additionto polymerases a andy, anyother proteins requiring a sulfhydryl group for activity would be inactivated.Nonetheless, repair synthesis induced by MNNG, NMU, and UV irradiation were much more sensitive to NEM inhibition than was repair synthesis induced by bleomycin. The similar sensitivity of repair synthesis in rodent indicates th atdifferences in cell species was not theorigin of the conflicting reports.Differences in salt concentrations employed insi tu has also   been shown not to alter the extent to which polymerase inhibitors reduce repair synthesis. Theextent of involvement of different polymerases in DNA repair synthesis appears to be related to the agent used to damage DNA.These cells did not contain polym erase Y and may be viewed asatypical or special cells.At least three factors may be involved in determining which polymerase participates in repair synthesis theamount of DNA damage, the patch size of repaired DNA and the actual type of damage being repaired.The size of DNA resyn thesized af ter damage by some agents, such asX irradiation, is relatively small a re synthesized in response to agents such asUV irradiation. We offer an alternative explanation of our findings.During repair of many types of DNA damage, inci sion processes create and termini on damaged DNA strands which are susceptible to typical repair nucleases.On the other hand, bleomycin and neocarzinostatin crea te breaks in DNA which may not be susceptible to thesame repair nucleases.After bleomycin trea tment, the end of the brokenstrand is blocked by a CHCHCOOH group, and following neocarzinostatintrea tment, the end appearsto be blocked by a residual sugar moiety. Such blocked termini may not be subs tra tes for typical repair nucleases.Repair of dam aged DNA containing blocked termini may require excision of blocked termini by a polymerase associated nuclease, fol lowed by resynthesis primarily, butnot necessarily exclu sively, with polymerase p.Preparation of insi tu cell systems may alter initiation of normal repair processes in some fashion, causing DNA polymerases to par ticipate differently in repair synthesis.It will be imperativeto investigate th is possibility to determine whether insi tu SYS tems are valid models for studying DNA repair synthesis.M ll lerand. Ne ChlnaultuM N E M More DNA dam age was induced by the alkylating agents than by bleo mycin or neocarzinostatin, suggesting that the extent of involvement of polymerase a or in DNA repair synthesisis related to the amount or type of DNA damage.In <a href="http://www.targetmol.com/compound/Montelukast">buy Montelukast</a> addition, salt concentration was found to have little or no effect on the results obtained with the DNA polymerase inhibitors.Our findings provide an explanation for conflicting reports in the literature concerning the roles of DNA polymerases a and in DNA repair.Mammalian cells con ta in three DNA polymerases desig na ted a, and y, and the function of each polymerasehas been the sub jectof many studies.Po lymeraseyis involved in mi tochondr ial DNA replication. Po lymerase a is largely responsible for repli cating nuc lear DNA. However, recentstud ies utilizing in situ sys tems have led to con troversy regardingtherole of polym erases a and in repa ir syn thes is.

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