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1 Pol zeta also includes REV7 subunits (encoded by Rev7 in
2 Pol zeta also participates in repair by microhomology me
3 Pol zeta is an error-prone DNA polymerase that is critic
4 Pol zeta is particularly error prone for substitutions i
5 Pol zeta is relatively accurate for single base insertio
6 Pol zeta is unique amongst TLS polymerases for its essen
7 Pol zeta is used in response to circumstances that stall
8 Pol zeta is very inefficient in inserting deoxynucleotid
9 Pol zeta, however, is unusually sensitive to geometric d
10 Pol zeta-deficient B cells had a reduction in mutation f
14 s occur by the exchange of the Pol delta and Pol zeta catalytic subunits on a preassembled complex of
15 similar C-terminal domains of Pol delta and Pol zeta contain a [4Fe-4S] cluster coordinated by four
17 usively directed G->A mutations; Pol eta and Pol zeta participated in error-prone bypass of the strai
18 ra indicates a hierarchy between Pol eta and Pol zeta with respect to the bypass of UV-induced lesion
21 Also, we provide evidence that Pol kappa and Pol zeta function together in promoting error-free repli
23 ation fork to generate a first mutation, and Pol zeta extends the mismatch with a second mutation.
24 eracts with Y-type DNA polymerases (Pol) and Pol zeta to bypass many types of adducts that block the
25 died the ability of Y-family polymerases and Pol zeta to bypass ICLs that induce different degrees of
27 cells utilize both DNA gap filling (REV1 and Pol zeta) and replicative (Pol delta) DNA polymerases to
29 by reversion of the lys2deltaA746 allele, as Pol zeta produces a distinct mutational signature in thi
32 w that although Pol32 does not directly bind Pol zeta, Pol32 can bind the Rev1-Pol zeta complex throu
33 ther by Rev1 in the Rev1-Pol32 complex or by Pol zeta in the Pol zeta-Rev1-Pol32 complex, irrespectiv
35 gesting that low-fidelity DNA replication by Pol zeta is at least partly responsible for the MNMs tha
37 er involvement of mutagenic DNA synthesis by Pol zeta as well as diminished proofreading by Pol delta
40 cell nuclear antigen (PCNA)-dependent TLS by Pol zeta as Pol zeta(2) lacks functional interactions wi
43 erein, we show that Saccharomyces cerevisiae Pol zeta binds to the Pol31 and Pol32 subunits of Pol de
44 t the properties of Saccharomyces cerevisiae Pol zeta in which phenyalanine was substituted for the c
46 n found to physically interact with Pol eta, Pol zeta, and Rev1, suggesting a possible role of PolDIP
48 onger version, found naturally in eukaryotic Pol zeta (a family-B translesion synthesis polymerase).
49 uirement of Rev1 as a structural element for Pol zeta and not for Pol eta, these observations have ra
51 al significance of Rev1 binding to Pol32 for Pol zeta function in TLS and suggest a structural role f
54 ough AT-rich hairpins and suggest a role for Pol zeta in rescue of stalled replication forks caused b
56 onsisting of the Rev1 CTD, the heterodimeric Pol zeta complex, and the Pol kappa Rev1-interacting reg
58 polymerase epsilon, whereas yeast and human Pol zeta efficiently synthesize these regions in a stepw
62 o decipher the bases of Pol32 involvement in Pol zeta-mediated TLS, here we examine whether Pol32 phy
63 v1 plays an indispensable structural role in Pol zeta-dependent lesion bypass, the role of its DNA sy
64 v1 plays an indispensable structural role in Pol zeta-mediated TLS and it binds the Rev3 catalytic su
73 ches, whereas knock-in mice with a mutagenic Pol zeta displayed a marked increase in mutation frequen
75 l role for Rev1 in modulating the binding of Pol zeta with Pol32 in Pol delta stalled at a lesion sit
78 ed, suggesting that the proposed function of Pol zeta as an extender DNA polymerase is also required
79 ermutation, we generated two mouse models of Pol zeta function: a B cell-specific conditional knockou
81 r results, we suggest a nonredundant role of Pol zeta in DNA DSB repair through nonhomologous end joi
82 the data thus argue against a direct role of Pol zeta in SHM, Pol zeta deficiency directly interfered
83 RNA-DNA recombination, uncovering a role of Pol zeta in transferring genetic information from transc
85 bstitution in Rev3, the catalytic subunit of Pol zeta, are nearly UV immutable, suggesting severe los
91 results showed that deficiency in Pol eta or Pol zeta, but not Pol kappa or Pol iota, led to pronounc
92 ic cells deficient in Pol kappa, Pol iota or Pol zeta, suggesting the mutual involvement of multiple
93 replication stress, and PARP1/2-trapping or Pol zeta inhibitor-induced gammaH2AX foci accumulation i
94 reviously shown following targeting of other Pol zeta-proteins, suggesting that Pol zeta-dependent an
97 tion is combined with that of DNA polymerase Pol zeta, which is essential for damage-induced mutagene
99 d: silencing the Rev3l subunit of polymerase Pol zeta to impair DNA repair in combination with cispla
100 e the spectrum of the error-prone polymerase Pol zeta, suggesting that low-fidelity DNA replication b
102 with Rev1 and the error-prone TLS polymerase Pol zeta, and elevates mutagenesis that relies on POLD3,
105 ly with Rev7 (a subunit of a TLS polymerase, Pol zeta) and with two other Y-family polymerases, Pol i
106 yeast translesion synthesis DNA polymerases Pol zeta and Pol eta in UV survival and mutagenesis were
109 n indispensable structural role in promoting Pol zeta function, and deletion of the Rev1-C terminal r
111 TLS are three DNA polymerases (Pols): Rev1, Pol zeta (Rev3/7), and Pol eta (Rad30), all with human h
115 nt depends on Pol eta and the Pol kappa-REV1-Pol zeta polymerase complex and introduces predominantly
116 ectly bind Pol zeta, Pol32 can bind the Rev1-Pol zeta complex through its interaction with Rev1.
118 negatively regulates POLD3 function in Rev1/Pol zeta-dependent TLS, revealing a previously unrecogni
120 ue against a direct role of Pol zeta in SHM, Pol zeta deficiency directly interfered with CSR in that
122 fective pol30-113 mutant, fails to stimulate Pol zeta(4) activity, providing an explanation for the o
124 te pathways for mutagenic TLS, surprisingly, Pol zeta functions independently of these Pols and in a
125 tiple positions along the BIR track and that Pol zeta is responsible for the majority of both spontan
128 e studies performed in vivo, we propose that Pol zeta is the major DNA Pol that functions in the RNA-
131 of other Pol zeta-proteins, suggesting that Pol zeta-dependent and -independent roles of Rev7 are re
132 nesis in nondividing cells occurs during the Pol zeta-dependent filling of lesion-containing, NER-gen
134 the Rev1-Pol32 complex or by Pol zeta in the Pol zeta-Rev1-Pol32 complex, irrespective of whether pro
135 e, we show that the C-terminal domain of the Pol zeta catalytic subunit interacts with accessory subu
136 that the complex events are dependent on the Pol zeta translesion polymerase, thus implicating the DN
143 ol zeta is error-prone compared to wild-type Pol zeta, providing a biochemical rationale for the obse
144 Thus L979F Pol zeta, and perhaps wild-type Pol zeta, which also generates clustered mutations at a
148 rporates a C opposite this adduct from which Pol zeta subsequently extends, thereby completing the le
149 sions occurs when Pol delta is combined with Pol zeta, indicating a role for Polzeta in extending fro
150 city of pol zeta in vitro is consistent with Pol zeta-dependent mutagenic specificity reported in viv
151 mine whether Pol32 physically interacts with Pol zeta or its associated proteins and provide evidence
153 that human Pol iota and a two-subunit yeast Pol zeta complex (REV3/REV7) could function efficiently
157 FS FRA16D, we find that DNA polymerase zeta (Pol zeta) is required to prevent breakage and subsequent
159 nscriptase, translesion DNA polymerase zeta (Pol zeta) plays a major role in R-TDR, and it is essenti
161 nthesis (TLS) together with polymerase zeta (Pol zeta), comprised of the Rev3 catalytic and Rev7 acce
163 roteins are subunits of DNA polymerase-zeta (Pol-zeta), an enzyme whose sole function appears to be t