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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
11 tional knockout and a knock-in strain with a Pol zeta mutagenesis-enhancing mutation.
12 he assembly of the [4Fe-4S] cluster abrogate Pol zeta function in UV mutagenesis.
13              With a tagged form of an active Pol zeta variant, we isolated two additional accessory s
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
16                             Both Pol eta and Pol zeta extended the DL more efficiently than Pol delta
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
19 and DNA polymerase (Pol) delta, Pol eta, and Pol zeta.
20         Additionally, Pol eta, Pol iota, and Pol zeta, but not Pol kappa, had important roles in prom
21 Also, we provide evidence that Pol kappa and Pol zeta function together in promoting error-free repli
22 s deoxynucleotides opposite DNA lesions, and Pol zeta functions as a mispair extender.
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
26  and describe the specific roles of Rev1 and Pol zeta in handling these disturbances.
27 cells utilize both DNA gap filling (REV1 and Pol zeta) and replicative (Pol delta) DNA polymerases to
28 s mutagenesis that relies on POLD3, Rev1 and Pol zeta.
29 by reversion of the lys2deltaA746 allele, as Pol zeta produces a distinct mutational signature in thi
30  antigen (PCNA)-dependent TLS by Pol zeta as Pol zeta(2) lacks functional interactions with PCNA.
31                      For all other DNA bases Pol zeta is essential for ROS-induced mutagenesis.
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
34 tes are comparable with replication rates by Pol zeta on undamaged DNA.
35 gesting that low-fidelity DNA replication by Pol zeta is at least partly responsible for the MNMs tha
36 nslesion synthesis of a model abasic site by Pol zeta.
37 er involvement of mutagenic DNA synthesis by Pol zeta as well as diminished proofreading by Pol delta
38 p did not stimulate translesion synthesis by Pol zeta or by DNA polymerase delta.
39 er termini and extension of these termini by Pol zeta.
40 cell nuclear antigen (PCNA)-dependent TLS by Pol zeta as Pol zeta(2) lacks functional interactions wi
41  required for translesion synthesis (TLS) by Pol zeta.
42  a terminus that was extended efficiently by Pol-zeta, but not by yeast Pol-alpha.
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
45         The translesion polymerases Pol eta, Pol zeta, and Rev1 are part of a suite of factors in yea
46 n found to physically interact with Pol eta, Pol zeta, and Rev1, suggesting a possible role of PolDIP
47 hfully inserted across the ICL-G by Pol eta, Pol zeta, and Rev1-Pol zeta.
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
50 ns at AT/TA repeats suggests a mechanism for Pol zeta recruitment.
51 al significance of Rev1 binding to Pol32 for Pol zeta function in TLS and suggest a structural role f
52                      So far, such a role for Pol zeta has been established for cyclobutane pyrimidine
53          Our results reveal a novel role for Pol zeta in replicating through AT-rich hairpins and sug
54 ough AT-rich hairpins and suggest a role for Pol zeta in rescue of stalled replication forks caused b
55                                 Furthermore, Pol zeta, but not Pol eta, also contributes to 4-NQO res
56 onsisting of the Rev1 CTD, the heterodimeric Pol zeta complex, and the Pol kappa Rev1-interacting reg
57 on of a minimally catalytically active human Pol zeta variant.
58  polymerase epsilon, whereas yeast and human Pol zeta efficiently synthesize these regions in a stepw
59 d two additional accessory subunits of human Pol zeta, PolD2 and PolD3.
60                        Amino acid changes in Pol zeta that prevent the assembly of the [4Fe-4S] clust
61 ct or the abasic sites as those deficient in Pol zeta or Rev1.
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
65  physical interactions with Rev3 inactivates Pol zeta function in TLS.
66                                        L979F Pol zeta also generates multiple errors in close proximi
67                                        L979F Pol zeta shares with wild-type Pol zeta the ability to p
68                    Errors generated by L979F Pol zeta in vitro include single-base insertions, deleti
69            When copying undamaged DNA, L979F Pol zeta is error-prone compared to wild-type Pol zeta,
70                  We show that purified L979F Pol zeta is 30% as active as wild-type Pol zeta when rep
71                                   Thus L979F Pol zeta, and perhaps wild-type Pol zeta, which also gen
72                                At a minimum, Pol zeta consists of a catalytic subunit Rev3 and an acc
73 ches, whereas knock-in mice with a mutagenic Pol zeta displayed a marked increase in mutation frequen
74 e for Pol kappa at the insertion step and of Pol zeta at the extension step of Tg bypass.
75 l role for Rev1 in modulating the binding of Pol zeta with Pol32 in Pol delta stalled at a lesion sit
76                    In addition, depletion of Pol zeta resulted in significant decreases in T-->C muta
77 er in Rev3 is essential for the formation of Pol zeta(4) and damage-induced mutagenesis.
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
80 f Pol kappa, and for O6-CMdG upon removal of Pol zeta.
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
84 tations that represent a unique signature of Pol zeta.
85 bstitution in Rev3, the catalytic subunit of Pol zeta, are nearly UV immutable, suggesting severe los
86 ), we ablated Rev3, the catalytic subunit of Pol zeta, selectively in mature B cells in vivo.
87 sensus motif is lacking in either subunit of Pol zeta, yet its activity is stimulated by PCNA.
88  REV3 gene encoding the catalytic subunit of Pol zeta.
89 n the gene encoding the catalytic subunit of Pol zeta.
90 S and it binds the Rev3 catalytic subunit of Pol zeta.
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
95                         However, on its own, Pol zeta is highly inefficient at replicating through DN
96              Rev1-Pol zeta, and particularly Pol zeta alone showed a tendency to stall before the ICL
97 tion is combined with that of DNA polymerase Pol zeta, which is essential for damage-induced mutagene
98 enesis by the fourth B-family DNA polymerase Pol zeta.
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
101  resectioning and the error-prone polymerase Pol zeta.
102 with Rev1 and the error-prone TLS polymerase Pol zeta, and elevates mutagenesis that relies on POLD3,
103 tching involving REV1 and the TLS polymerase Pol-zeta.
104 generated by another error-prone polymerase, Pol zeta.
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
107  it is particularly important for preventing Pol zeta-dependent mutagenesis at tRNA genes.
108                                     To probe Pol zeta functions in vivo via its error signature, here
109 n indispensable structural role in promoting Pol zeta function, and deletion of the Rev1-C terminal r
110                              The error-prone Pol zeta can also participate in replication of undamage
111  TLS are three DNA polymerases (Pols): Rev1, Pol zeta (Rev3/7), and Pol eta (Rad30), all with human h
112                                         Rev1-Pol zeta, and particularly Pol zeta alone showed a tende
113 oss the ICL-G by Pol eta, Pol zeta, and Rev1-Pol zeta.
114                          No stalling by Rev1-Pol zeta directly past the ICL was observed, suggesting
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.
117                                     The Rev1-Pol zeta complex was most efficient in complete bypass s
118  negatively regulates POLD3 function in Rev1/Pol zeta-dependent TLS, revealing a previously unrecogni
119 ithin this group, including RAD5, REV3/REV7 (Pol zeta), RAD30 (Pol eta), and POL30 (PCNA).
120 ue against a direct role of Pol zeta in SHM, Pol zeta deficiency directly interfered with CSR in that
121                                     A stable Pol zeta(4) complex can be identified in all phases of t
122 fective pol30-113 mutant, fails to stimulate Pol zeta(4) activity, providing an explanation for the o
123 ubunits of Pol delta, forming a four-subunit Pol zeta(4) complex (Rev3-Rev7-Pol31-Pol32).
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
126                                 We find that Pol zeta reverse transcriptase activity is not affected
127                                We found that Pol zeta is very inefficient at inserting nucleotides op
128 e studies performed in vivo, we propose that Pol zeta is the major DNA Pol that functions in the RNA-
129                                 We show that Pol zeta/Rev1-dependent mutations occur at sites of repl
130                    The comparison shows that Pol zeta far surpasses Pol eta and all other DNA Pols in
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
133 hesis (TLS) by releasing it from REV3 in the Pol zeta complex.
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
137 se sequences that is primarily used when the Pol zeta/Rev1-dependent pathway is inactive.
138                                        Thus, Pol zeta is a highly specialized polymerase that can pro
139 ile others have suggested that the yeast TLS Pol zeta is involved.
140 e bypass synthesis, by 2-3 fold, compared to Pol zeta alone or Pol eta.
141         L979F Pol zeta shares with wild-type Pol zeta the ability to perform moderately processive DN
142 L979F Pol zeta is 30% as active as wild-type Pol zeta when replicating undamaged DNA.
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
145                       To date, no vertebrate Pol zeta has been purified for biochemical characterizat
146 otide insertion opposite the lesion, whereas Pol zeta executes the extension step.
147                     Here, we examine whether Pol zeta can replicate through the 7,8-dihydro-8-oxoguan
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
152                                        Yeast Pol zeta and human Pol kappa generated distinct mutation
153  that human Pol iota and a two-subunit yeast Pol zeta complex (REV3/REV7) could function efficiently
154                         DNA polymerase zeta (Pol zeta) and Rev1 are essential for the repair of DNA i
155                         DNA polymerase zeta (Pol zeta) and Rev1 are key players in translesion DNA sy
156                         DNA polymerase zeta (Pol zeta) is a eukaryotic B-family DNA polymerase that s
157 FS FRA16D, we find that DNA polymerase zeta (Pol zeta) is required to prevent breakage and subsequent
158                         DNA polymerase zeta (Pol zeta) plays a key role in DNA translesion synthesis
159 nscriptase, translesion DNA polymerase zeta (Pol zeta) plays a major role in R-TDR, and it is essenti
160                         DNA polymerase zeta (Pol zeta), a heterodimer of Rev3 and Rev7, is essential
161 nthesis (TLS) together with polymerase zeta (Pol zeta), comprised of the Rev3 catalytic and Rev7 acce
162 on bypass together with DNA polymerase zeta (Pol zeta).
163 roteins are subunits of DNA polymerase-zeta (Pol-zeta), an enzyme whose sole function appears to be t

 
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