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Fission yeast Rad8-dependent PCNA ubiquitination at lysine 107 promotes gross chromosomal rearrangements

蘇, 傑 大阪大学 DOI:10.18910/85277

2021.06.23

概要

Faithful repair of DNA damage is crucial for maintaining genome integrity. Spontaneous double strand breaks (DSBs) and stalled replication forks can induce homologous recombination (HR). HR is considered as an error-free DNA repair mechanism, as it uses intact homologous DNA as the template. However, homologous recombination can occur between ectopic sites from repetitive sequences and when accompanied with crossover or through break-induced replication (BIR), can lead to gross chromosomal rearrangements (GCRs). GCRs, such as deletion, translocation, and inversion, can cause cell death and diseases including cancer. However, how GCRs occur remains unclear. Rad51 recombinase, a key HR factor, catalyzes DNA strand exchange with homologous duplex DNA molecules. Rad51 promotes gene conversion, a non-crossover type of recombination. Loss of Rad51 reduces gene conversion causing the DNA damage be repaired by GCRs. In fission yeast, loss of Rad51 greatly increases the formation of isochromosomes and truncation. Isochromosomes that contain mirrorimaged arms formed between centromere inverted repeats. Truncations formed by addition of de novo telomeres to broken ends. Yeast Rad52 promotes Rad51 loading onto DNA, but this function is not conserved in mammals. Both yeast and mammalian Rad52 catalyzes single-strand annealing (SSA) of complementary single-stranded DNA (ssDNA) molecules. SSA is independent of Rad51. Rad52- dependent SSA can cause GCRs, as the rad52-R45K mutation, which impairs SSA in vitro, largely reduces isochromosome formation in rad51∆ cells. Mus81, a crossover-specific endonuclease is required for Rad52-dependent GCRs probably by cleaving the joint molecule formed by Rad52 to crossover products. Rad52-dependent SSA can also lead to gene conversion, but Mus81 is not required for gene conversion. Does the recruitment of Mus81 determines the fate of the joint molecule leading to GCRs, but not gene conversion? The detailed mechanism of Rad52-dependent GCRs remains unclear.

Here, I provide genetic evidence that fission yeast Rad8 and Mms2-Ubc4 E2 conjugating enzymes catalyze PCNA lysine 107 (K107) ubiquitination to promote Rad52-dependnet GCRs. Rad8 E3 ligase is the homolog of budding yeast Rad5 and human HLTF. Using an extra chromosome, ChLC to monitor GCRs in fission yeast, I found that loss of Rad8 reduced GCRs in rad51Δ cells. Two types of GCRs were detected using ChLC in rad51∆ cells: isochromosome and truncation. rad8Δ reduced 75% of the isochromosomes formed in rad51Δ cells, but did not affect chromosomal truncations, showing that Rad8 is specifically required for homology-mediated GCRs. Rad8 contains three conserved domains: HIRAN, SNF2/SWI2 translocase, and RING finger domains. The HIRAN domain mediates binding to 3' ends of ssDNA. The translocase domain contains an ATP binding motif and catalyzes translocation on doublestranded DNA (dsDNA). The RING domain binds ubiquitin E2 enzyme and transfers ubiquitin from E2 to the substrate. Mutations in HIRAN and RING but not translocase domain of Rad8 reduced GCRs, suggesting that the abilities of Rad8 to bind the 3'-end of ssDNA and to catalyze ubiquitination are required for isochromosome formation. With the aid of Mms2-Ubc13 and Mms2-Ubc4 E2 ubiquitinconjugating complexes, Rad8 catalyzes ubiquitination of the same substrate, PCNA, but at different sites, K164 and K107, respectively. PCNA ubiquitination at K164 promotes a template switching pathway of DNA damage tolerance, while the role of ubiquitination at PCNA K107 is unclear. mms2 and ubc4, but not ubc13 reduced GCRs. PCNA K107R but not K164R reduced GCRs in rad51∆ cells. rad8-RING, ubc4, and PCNA K107R mutations reduced GCRs in epistatic manner, suggesting that, with the aid of Ubc4-Mms2, Rad8 ubiquitinates PCNA at K107 to promote GCRs. I also found that the rad52-R45K, mus81∆ and PCNA K107R mutations epistatically reduced the GCR rate, showing that PCNA K107 works with Mus81 in Rad52-dependent GCRs. PCNA is a homotrimer forming ring structure. K107 is located at the PCNA-PCNA subunits interface, raising the possibility that K107 ubiquitination weakens the subunits interaction. Remarkably, an interface mutation D150E greatly increased the GCR rate of pcn1-K107R cells, showing that the interface mutation bypasses the requirement of PCNA K107 in GCRs. D150E mutation also increased the GCR rate of rad8-RING cells, showing that the mutation bypasses Rad8 ubiquitination activity. Taken together, these results suggest that Rad8-Ubc4-Mms2- dependent PCNA K107 ubiquitination weakens PCNAPCNA subunits interaction to cause GCRs. I hypothesize that PCNA K107 ubiquitination destabilizes the PCNA trimer, which cause the sliding of PCNA to expose ssDNA that can used by Rad52- dependent SSA and/or make space for Mus81 recruitment. This study has uncovered a role of the noncanonical PCNA ubiquitination at K107 in Rad52- dependent GCRs.

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