A ROLE OF Caenorhabditis elegans polq-1 AND hel-308 IN DNA REPAIR By Dott. Diego Matteo Muzzini Genomes are daily challenged by different mutagens, which can seriously damage it. Since un-repaired DNA damage leads to apoptosis or cancer development, genomes evolved a number of different DNA repair pathways to face such damages. Among all possible DNA lesions, Interstrand Cross-Links (ICLs), which covalently bind the DNA strands together, are the most toxic ones. A number of evidences demonstrated that ICL could be repaired using Homologous Recombination (HR), Fanconi Anemia (FA) and Tranlesion Synthesis (TLS) pathways alone or in combination. Nevertheless, a precise mechanistic model is still lacking in eukaryotes and it is thought that many genes could be involved to overcome this kind of lesion. The Drosophila melanogaster gene mus-308 and spnC/mus301 are genes involved in DNA damage repair. I particulat they seems dedicated to ICLs lesions repair. In my PhD project I focused my effort to elucidate the role of polq-1 and hel-308, which are Caenorhabditis elegans orthologs of mus-308 and spnC/mus301, during ICL repair. Here I show that polq-1 and hel-308 are the functional homologues of mus-308 and spnC/mus301, respectively and they are necessary for DNA repair in worms. Moreover, polq-1 seems not to involved neither in homologous recombination (HR) nor in the Fanconi anemia (FA) pathways, while it synergically interacts with hel-308 in a non-linear pathway, probably also involving translesion DNA synthesis (TLS).
A role of Caenorhabditis elegans polq-1 and hel-308 in DNA repair
MUZZINI, DIEGO MATTEO
2006
Abstract
A ROLE OF Caenorhabditis elegans polq-1 AND hel-308 IN DNA REPAIR By Dott. Diego Matteo Muzzini Genomes are daily challenged by different mutagens, which can seriously damage it. Since un-repaired DNA damage leads to apoptosis or cancer development, genomes evolved a number of different DNA repair pathways to face such damages. Among all possible DNA lesions, Interstrand Cross-Links (ICLs), which covalently bind the DNA strands together, are the most toxic ones. A number of evidences demonstrated that ICL could be repaired using Homologous Recombination (HR), Fanconi Anemia (FA) and Tranlesion Synthesis (TLS) pathways alone or in combination. Nevertheless, a precise mechanistic model is still lacking in eukaryotes and it is thought that many genes could be involved to overcome this kind of lesion. The Drosophila melanogaster gene mus-308 and spnC/mus301 are genes involved in DNA damage repair. I particulat they seems dedicated to ICLs lesions repair. In my PhD project I focused my effort to elucidate the role of polq-1 and hel-308, which are Caenorhabditis elegans orthologs of mus-308 and spnC/mus301, during ICL repair. Here I show that polq-1 and hel-308 are the functional homologues of mus-308 and spnC/mus301, respectively and they are necessary for DNA repair in worms. Moreover, polq-1 seems not to involved neither in homologous recombination (HR) nor in the Fanconi anemia (FA) pathways, while it synergically interacts with hel-308 in a non-linear pathway, probably also involving translesion DNA synthesis (TLS).I documenti in UNITESI sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
https://hdl.handle.net/20.500.14242/76814
URN:NBN:IT:UNIMI-76814