Cajal bodies are centers of RNP-complex assembly for spliceosomal snRNPs and other RNPs

TLS Online TPP Program

#Id: 6146

#Unit 3. Fundamental Processes

TLS Online TPP Program

#Id: 6147

#Unit 3. Fundamental Processes

TLS Online TPP Program

#Id: 6148

#Unit 3. Fundamental Processes

TLS Online TPP Program

#Id: 6149

#Unit 3. Fundamental Processes

Ku70, Ku80, DNA-PKcs, Artemis, XRCC4, Cernunnos-XLF, and DNA ligase IV. Ku70 and Ku80 are the most fundamental components of NHEJ. 

They constitute a heterodimer that binds to the DNA ends and recruits DNA-PKcs, which is a protein kinase. DNA-PKcs, in turn, forms a complex with Artemis. Artemis is both a 5’-to-3’ exonuclease and a latent endonuclease that is activated by phosphorylation by DNA-PKcs. 

These nucleolytic activities process the broken ends and prepare them for ligation. Ligase IV performs ligation in a complex with XRCC4 and Cernunnos-XLF.

TLS Online TPP Program

#Id: 6150

#Unit 3. Fundamental Processes

H2AX phosphorylated at serine 129 in yeast, 139 in mammals) is referred to as g-H2AX. g-H2AX is a universal marker for double strand breaks

TLS Online TPP Program

#Id: 6151

#Unit 3. Fundamental Processes

Even if cells cannot repair these lesions, there is a fail-safe mechanism that allows the replication machinery to bypass these sites of damage or tolerate the DNA damage. One mechanism of DNA damage tolerance is translesion synthesis. Although this mechanism is, as we shall see, highly error-prone and thus likely to introduce mutations, translesion synthesis spares the cell the worse fate of an incompletely replicated chromosome. A key feature of DNA damage tolerance is that the DNA lesion remains in the genome. DNA repair pathways can subsequently correct the lesion.