1. Drosophila Pol32 Pif1 Double Mutants Show
Increased Aborted SDSA in P- Element
Excision Repair
David Grossfeld: Bio 194
Research done in the McVey Lab
Research advisor: Sarah Dykstra
45 Sunset Road
Somerville, MA 02155
I have read this report:

2. Abstract
The PIF1 5’ to 3’ helicase and Pol Delta subunit of POL32 have shown to be required for
extensive synthesis in yeast homologous recombination. When both genes are deleted, yeast cells
die. This has led to studies of the single mutants in Drosophila through the P{w}a assay, which
gives insight into the type of DNA which can be differentiated through eye color via repair of a
double-stranded break. One study through Pif1 found that synthesis up to 9 kb increased in
mutants compared to wildtype, while another study of the pol32L2 mutant showed that synthesis
decreased all together compared to wildtype. Due to these contrasting results, we look to
examine the double mutant Pif1Pol32. We have found that these flies can survive and
reproduce, unlike in yeast. More importantly, how efficiently can these flies repair a double
strand break compared to the single mutants, and in what pathway(s)? We use a p element
excision and repair assay to explore the behavior of the double mutant in DNA double-strand
break repair.
Introduction
In Drosophila melanogaster, the integrity of the genome is crucial to its function,
growth, development, and reproduction. Exogenous damage such as chemical mutagens,
genotoxic agents, and UV radiation, as well as endogenous damage due to reactive oxygen
species or replication fork collapse, may lead to double strand breaks within the DNA. These
breaks can be potentially lethal, and if not repaired or repaired incorrectly can lead to cell
death or even cancer. (McVey et al). Drosophila are capable of coding for DNA repair proteins
that can repair double strand breaking-inducing lesions. Homologous recombination (HR), a
type of DNA repair, uses a homologous DNA template to repair the broken chromosome, as
opposed to Non-Homologous End Joining, which ligates the end of the break together without
using a template or external homologies (McVey et al).
One type of HR, SDSA, use 3’ single stranded DNA to invade the repair template and
synthesize new DNA, migrating across the gap via a displacement loop. The newly synthesized
DNA displaced and anneals back to the broken template. This results in repair via gene

3. conversion, which occurs when sequences on the broken chromosome and repair template
become identical after repair (Adams, McVey 2003).
In Drosophila, the excision of a p element in the P{w}a assay can be used to test the
efficiency of homologous recombination, specifically synthesis-dependent strand annealing
(SDSA). The P{w}a assay allows for the study of the factors involved in repair by SDSA. The
element contains the copia retrotransposon which is flanked by 276 -bp Long Terminal Repeats
(LTRs) and disrupts expression of the otherwise WT White gene. The copia retrotransposon is
inserted within the White gene located on the X chromosome. This construct is inserted into
the essential Scalloped gene, and a wild type fly has apricot colored eyes due to the insertion of
copia disrupting the white gene. A transposase excises the P{w}a transposable element,
allowing excision and repair events in both the soma and male germline.
Following excision and repair in the male germline, the type of repair can be determined
based on the eye color of the female progeny, which contain one intact copy of the p{w}a
obtained from the female and the P{w)a which has excised and repaired from the male.
Complete HR through the Copia retrotransposon or no excision results in an apricot eye color in
the female progeny, while sufficient homologous repair extending Into the LTR followed by
annealing of the broken ends results in WT expression of the White gene and a Red eyed
phenotype. In contrast, aborted HR resulting in very limited strand invasion or repair via End
Joining results in a yellow eyed phenotype.
In somatic tissues repair can be observed in the eyes of the fly because the transposase
can actively excise the p element on the x chromosome which contains the White eye color
gene. Perfect repair of the element produces apricot eyes, synthesis of 9 kb through the white

4. gene and annealing at the LTR’s produces red eyes, and incomplete HR or end joining produces
yellow eyes (Adams,McVey et al 2003). Because this assay measures the efficiency of DNA
repair, it can also measure whether the deletion of DNA repair genes affects repair products.
Two genes involved in homologous recombination are Pif1 and Pol32. The Pif1 gene is a
5’ to 3’ helicase which acts by reducing topological constraint of the migrating D-loop , while
Pol32 is a nonessential subunit of Polymerase Delta and Polymerase Zeta, involved in extensive
synthesis during HR. It has previously been shown that pif1167 single mutant flies in Drosophila
show an increase in synthesis through the entire white gene via the P{w}a assay, while synthesis
tract lengths decreased compared to wild type (Rodgers 2015). Furthermore, via the same
assay, pol32L2 null Drosophila mutants are significantly impaired in extensive synthesis during
HR compared to wild type (Kane, McVey 2012). In yeast, these genes may be synthetic lethal in
certain genetic backgrounds, indicating that these genes may act in redundant, but mutally
essential pathways.
However, it is unclear in Drosophila whether Pif1 and Pol32 act similarly to the results
observed in yeast or whether these genes play alternative roles in HR. Given the results
observed in the single mutants in Drosophila, we sought to answer the question of whether or
not the Pif1 and Pol32 genes act in the same repair pathway, and so a double mutant stock was
generated. In this experiment, we look to observe the efficiency of DNA repair in a
𝑝𝑖𝑓1𝑝𝑜𝑙32
𝑝𝑖𝑓1𝑝𝑜𝑙32
background, and give insight into the pathways that both genes are involved.
Materials and Methods
Balanced Stock Setup

5. After mentor Sarah Dykstra generated the double mutant stock, I set up 5 vials of stock 1
(renamed from stock D) containing one
pol32pif1
pif1pol32
and 6
pin
cyo
, as well as 7 vials of stock 2
(renamed from stock P’)
pol32pif1
pif1pol32
;
tm3
tm6b
with the same ratio of males to females. Eggs were
laid and after 2 days, males were removed from each vial, and the DNA was prepared for PCR
to confirm the double mutant.
Single fly DNA preps for PCR
50 ul of squishing buffer was used per fly, and 1 ul of proteinase K was added from frozen stock
(10 mg/ml). Squishing buffer was kept at room temperature. Next, each fly was placed in a .5
ml tube and mashed with a pipette tip containing 50 ul of the squishing buffer/proteinase K
combination. Finally, the proteinase K was inactivated by heating to 95 Celsius for 1-2 minutes.
PCR
There were 15 fly samples (wild type, pol32 control, pif1 control, 5 vials of Stock 1, 7 vials of
stock 2).
The PCR with primers outside of the deletion was performed to confirm the deletion of
pol32 and pif1. A second PCR using inside primers was performed to confirm the absence of the
wild type band for both deletions.
The first PCR performed used primers outside of both deletions, and the following
primers were used: In the pif1 master mix, the primers used were -666F and +2153 R, with wild

6. type band at 2.8kb and mutant band at 1.1 kb. In the pol32 master mix, the primers used were
2469R and -306F with a mutant band at 1.2 kb and wild type band was 2.8 kb.
The following primers were used for the PCR using a primer set running inside the
deletion site. The internal primers used for the pif1 deletion were -666F and +206 R, yielding a
wild type band at 800 base pairs The Pol32 internal primers -306F and 562 R, yield a wild type
band at 868 base pairs
Mating scheme for P{w}a assay
(1)
𝑦𝑤
𝑦𝑤
;
𝑝𝑖𝑛
𝑐𝑦𝑜
;
+
+
X
𝑤
𝑦
;
𝑇𝑀𝑆(2−3) 𝑟𝑦+
𝐷𝑟′
(2) w;
+
𝑐𝑦𝑜
;
+
𝑇𝑀𝑆(2−3) 𝑟𝑦+
X w;
𝑃𝑖𝑓1𝑝𝑜𝑙32
𝑝𝑖𝑓1𝑝𝑜𝑙32
;
+
+
(D1)
(3)
𝑤𝑃{𝑤}𝑎
𝑦
; ;
𝑝𝑖𝑓1𝑝𝑜𝑙32
𝑐𝑦𝑜
; X
𝑤
𝑦
;
𝑝𝑖𝑓1𝑝𝑜𝑙32
𝑐𝑦𝑜
;
+
𝑇𝑀𝑆(2−3) 𝑟𝑦+
(4)
𝑤𝑃{𝑤}𝑎
𝑦
;
𝑝𝑖𝑓1𝑝𝑜𝑙32
𝑝𝑖𝑓1𝑝𝑜𝑙32
;
+
𝑇𝑀𝑆(2−3) 𝑟𝑦+
X
𝑃{𝑤}𝑎
𝑃{𝑤}𝑎
(5)
𝑤𝑃{𝑤}𝑎
𝑤𝑃( 𝑤) 𝑎
;
+
𝑝𝑖𝑓1𝑝𝑜𝑙32
;
+
+
Figure 1. Shown is the mating scheme used to generate a pol32 pif1 double mutant containing
the p{w}a element on the X chromosome and transposase on the 3rd chromosome in generation
4. This male was then mated to a homozygous female containing the apricot p element, which
produced female progeny with one excision event from the father, and one wildtype p element
from the mother on the x chromosome.
As shown above, the D1 homozygous males were used to cross to w;
+
𝑐𝑦𝑜
;
+
𝑇𝑀𝑆(2−3) 𝑟𝑦+
, while the
D2 homozygous males were used to cross to W P{w}a;
𝑝𝑖𝑛
𝑐𝑦𝑜
. The final cross of
𝑤𝑃{𝑤}𝑎
𝑦
;
𝑝𝑖𝑓1𝑝𝑜𝑙32
𝑝𝑖𝑓1𝑝𝑜𝑙32
;
W P{w}a
𝑝𝑖𝑛
𝑐𝑦𝑜
X w;
𝑃𝑖𝑓1𝑝𝑜𝑙32
𝑝𝑖𝑓1𝑝𝑜𝑙32
(𝐷2)

7. +
𝑇𝑀𝑆(2−3) 𝑟𝑦+
males to the
𝑃{𝑤}𝑎
𝑃{𝑤}𝑎
female allows for recovery of female progeny that have one
wild type p element from the mother fly, as well as one p element with excision and repair from
the father.
Results
Confirming homozygous pif1167 pol32L2 stocks
Stock 1, obtained from Sarah Dykstra, contained flies that had the double mutant
genotype
𝑝𝑖𝑓1𝑝𝑜𝑙32
𝑝𝑖𝑓1𝑝𝑜𝑙32
. Two vials labeled D1and D2, each with one double mutant male, were
confirmed by PCR to be mutant for both Pol32 and Pif1. As shown below in figure 2, Pol32
stocks obtained from single male crosses D1 –D4, D5, P1, P3, and P5-P7 all show a 1.3kb PCR
product indicative of the mutant allele. Furthermore, in figure 3, the gel image for the PCR
using pif1 primers D1-D5, P1, and P3 through P7 all show the 1.1 kb band for the 1.7 kb pif1
deletion. Based on both gel images, stocks D1 through D5 and P1, P3, and P5 through P7 stocks
contained the deletion.

8. Figure 2. Pol32 primers gel image of stocksD1 through D5, as well asP1 throughP7. Stock D and Stock
P representtwodifferentcross-onstocks,inwhichmeioticrecombinationgeneratedachromosome
withboththe pif1 and pol32 deletion.The controlsconsistedof awildtype fly,singlemutantpol32and
single mutantpif1,inthatorder. Clearly,StocksP2 andP4 show no deletionof Pol32.
Figure 3. Pif1primergel image of stocksD1 throughD5, as well asP1 throughP7. Again,the controls
consistedof a wildtypefly,pol32single mutant,andpif1singlemutant,inthatorder.Here, stockP2
appearsto not containthe properdeletion,asnoband at 1.1 Kbexists. Asexpected,the pol32single
mutantcontrol columnshowsno bandat 1.1kb, but rather a faint2.8kb WT band.
In Figure 4, the gel image for pol32 primers, stocks D1, D2, D4, P1, and P5 show the
deletion. Figure 5 shows the results of the PIF1 PCR that would detect the presence of the WT
band. Importantly, this time the lack of a wild-type band reveals that the deletion was present
as shown in isolates D1, D2, D4, and P1 through P4.

9. Figure 4. Shown is the Pol 32 PCR gel image. The control stocks remain the same order as
previous. In this case, stocks D1, D2, D4, P5, and P1 show a deletion. Note that stocks D5 and P5
are switched in order. Expectedly, pol32 single mutant control column shows no band.
Figure 5. Pif1primerPCRGel image of stocks D1 throughD5, as well asP1 through P7. StocksD1, D2,
D4 and P1 throughP4 showa deletion.Note thatstocksD5 and P5 are switched inorderagain.
Expectedly, pif1single mutantcontrol columnshowsnoband.
Homozygous Double mutant male flies are viable and fertile
Based on the results from all four PCRs, stocks D1 and D2 are homozygous pif1 pol32
double mutants. Molecularly confirming the pif1 pol32 mutant in these two stocks was
necessary to build the stocks to be used in the P{w}a assay. The other implication of these gel
images was the confirmation that double mutant males from stocks D1 and D2 are viable
despite having both mutant alleles. In yeast pif1 pol32 double mutant cells can not survive.
Pif1 Pol32 double mutant fliesshownsignificantdefectsinsomatic repair of excisedPelements

10. Figure 6. (A through C). Flies A through C have genotype
𝑤𝑃{𝑤}𝑎
𝑦
;
𝑝𝑖𝑓1𝑝𝑜𝑙32
𝑝𝑖𝑓1𝑝𝑜𝑙32
;
+
𝑇𝑀𝑆(2−3) 𝑟𝑦+
shown
in the 4th generation of the mating scheme in figure 1. Therefore, these flies have active
transposase on the 3rd chromosome with the P element on the x chromosome, and are
homozygous for deletions of Pif1 and Pol32. Fly A shows approximately two thirds white
pigment, with a third apricot pigment in the eye. Fly B shows a majority of apricot pigment in
the eye with a narrow streak of white pigment through the midsection. Fly C shows about one
third red pigment, one third white pigment, and one third apricot pigment. (D) Fly D has
genotype
𝑤𝑃{𝑤}𝑎
𝑦
;
𝑝𝑖𝑓1𝑝𝑜𝑙32
𝑐𝑦𝑜
;
+
𝑇𝑀𝑆(2−3) 𝑟𝑦+
. This fly still has an active transposase and contains a p
element, but on the second chromosome has one wild type chromosome and 1 mutant
chromosome. (E) Fly E is a wild type fly homozygous for the p element on the x chromosome.
Generation 5 females show a majority of incomplete SDSA events
Preliminary data show that females collected in the 5th generation shown in Figure 1 with
genotype
𝑤𝑃{𝑤}𝑎
𝑤𝑃( 𝑤) 𝑎
;
+
𝑝𝑖𝑓1𝑝𝑜𝑙32
;
+
+
show yellow eyes in the majority. Yellow eyes suggest incomplete

11. SDSA in the excision event passed through the male germ line and into one of the X
chromosomes of the female progeny.
Table 1. Shown are the 5th generation females collected so far, with 68% of the progeny being
yellow with the excision event from the double mutant father. As shown below, very few
females have been collected containing the excision event from the heterozygous double
mutant father.
Column1 Double Mutant father Heterozygous mutant father
yellow 54 2
apricot 25 2
red 0 0
From this data, we see a pattern of incomplete SDSA in the female progeny to a larger
extent than has been observed in the past. Previous experiments using p element excision
repair have shown that he transposase usually cuts with a frequency of about 20%. These data
suggest that the transposase must cut at least 70% of the time to produce that percent yellow
eyed females with incomplete HR repair. We can suggest, from these results, that the
transposase may have been cutting at 80% efficiency in the past as well. Perhaps apricot
colored females were not products of no excision, but rather perfect repair through the entire p
element.
Discussion
Relating the 𝑝𝑖𝑓1 𝑝𝑜𝑙32 mutant to PIF1 and POL32 Drosophila single mutants in P{w}a assay
The P{w}a assay can provide insight into the mechanistic details of the role of genes of interest
in gene conversion, based on eye color, that occurs within mutants when subjected to a DNA
double-strand break. The same assay that I used was used to study repair in single mutant Pif1
flies and single mutant pol32L2 flies.

12. Based on data obtained so far, the pif1167 single mutant, through the P{w}a assay, may
not have in fact shown increased synthesis through the white gene in SDSA due to observed
increased annealing at the LTR’s, but actually less overall repair and fewer apricot (perfect
repair) events. There may be more red eyed flies, but this can be due to the fact that less
apricot flies were produced because of decreased synthesis in SDSA compared to wild type.
(Rodger, Kasey. Master’s Thesis 2015). In contrast, in pol32L2 single mutants, SDSA dropped
72%, while left end synthesis dropped off significantly around 2.5 Kb of repair (Kane, McVey
2012).
The
𝑤,𝑝{𝑤}𝑎}
𝑦
;
𝑝𝑖𝑓1𝑝𝑜𝑙32
𝑝𝑖𝑓1𝑝𝑜𝑙32
;
+
𝑇𝑀𝑆(2−3) 𝑟𝑦+
male from generation was able to hatch and
reproduce, as opposed to the double mutant in yeast that could not survive (unpublished,
Haber). This suggests that the presence of both genes in Drosophila is not essential to the
survival of the fly, although the absence of both genes affects DNA repair. Due to the P{w}a on
the X chromosome, the males were able to exhibit differential pigment coloring in the eye
when the tranposase excised this p-element. In the male germline the transposase is active and
is capable of excising the p{w}a p-element. For this reason, males with somatic transposase
expression exhibit random excision events throughout the eye. Yellow pigment forms due to
incomplete SDSA, red eyes form due to synthesis of 9 kb through the white gene, and apricot
eyes result from precise repair or no excision.
In figure 6, the majority of white eye color in fly A suggests a tendency towards aborted HR
repair. The section of apricot in the upper third of the eye suggests there may be some ability
for precise repair as well. Looking at Fly B, there appears to be majority of apricot pigment and

13. therefore precise repair or no excision, but also a streak of white pigment, suggesting aborted
SDSA. The eye of Fly C exhibits multiple types of repair events. Patches of white, red, and
apricot fill the eye, meaning the cells in the eye have engaged in precise HR repair or no
excision, repair through the white gene (5kb) followed by annealing of the LTRs, and also
aborted SDSA. Compared to the double mutant flies, fly E, the wild type male containing the
same p element, shows a uniform apricot eye color with no sign of deficiency in DNA repair. In
the heterozygous
y
P{wa}
;
pif1pol32
cyo
;
+
TMS (2−3)99b,ry+
male, shown as fly D, yellow pigment is still
present , although there is an increase in red pigment. The heterozygous mutants should
phenocopy wild type flies, as a chromosome with wild type copies of Pif1 and Pol32 is
present. In the past, it has been observed that wild type flies exhibit a combination of red
and apricot pigment in the eye. Here, we see white and yellow pigment in the eye,
suggesting that heterozygotes may still be impaired in SDSA synthesis through the p
element. In
𝑤,{𝑝𝑤𝑎}
𝑦
;
𝑝𝑖𝑓1𝑝𝑜𝑙32
𝑝𝑖𝑓1𝑝𝑜𝑙32
;
+
𝑇𝑀𝑆(2−3) 𝑟𝑦+
male flies, qualitative data based on imaging and
observed flies suggest that incomplete SDSA is common in the homozygotes, along with some
level precise repair and full HR with annealing to the LTRs surrounding the Copia
retrotransposon. In both the pol32L2 and pif1167 single mutants, the increase in incomplete
repair (yellow eyes) was not statistically significant. In contrast, I see a qualitative increase in
the amount of incomplete HR repair in pol32 pif1 double mutant flies. This leads to the
question of whether or not both genes are involved in the same pathway in the P{w}a assay,
which provides a model for observing repair via SDSA, form of homologous recombination.
Inferring Possible Pathway of PIf1 and Pol32 in the Drosophila experimental model

14. In yeast experiments, it has been shown that Pol32 and PIF1 are required to complete
extensive synthesis in Homologous recombination, and deleting PIF1 results in increased half
crossovers and decreased synthesis. Furthermore, in S. cerevisiae, both the POL32 and PIF1
genes are involved partially, but not required, in the gene conversion pathway (SDSA). Deleting
POL32 reduces gene conversion by 25% (Lydeard et al). Without PIF1, Polymerase Delta can
only extend the invading strand approximately 200-500 nucleotides (Wilson et al.). In extensive
synthesis in yeast, PIF1 helicase is thought to reduce topological constraint on the D-loop in the
BIR, allowing polymerase delta to extend the single-stranded DNA. On the other hand, Pol32
interacts with PCNA and increases the efficiency of Polymerase Delta and Polymerase zeta
(Wilson et al).
In the Drosophila model, we have observed many cases of yellow and white pigment patches in
the eyes of the males expressing the somatic transposase. These findings suggest that there is
qualitatively less repair synthesis in the double mutant compared to the single mutants of both
genes Drosophila. As discussed previously, the pif1167 and pol32L2
single mutants did produce the same phenotypic results in the p{w}a assay. In fact, females with
the excision event in the pif1167 mutant background showed increased annealing at LTR’s (full
HR) and overall decrease in synthesis tract lengths compared to wild type, while pol32L2 single
mutants showed a decrease in LTR annealing. If we make an assumption that both genes act in
independent pathways, it would make sense as to why such a severe phenotype is being
observed in the double mutant males. If both genes act in separate pathways, deleting both
would negatively affect DNA repair to an even larger extent. This leads to the preliminary data

15. collected of female progeny in the 5th generation, which contain one excision event from the
father and one wild type p element from the mother.
Due to the randomness with respect to the timing of excision and repair within the
male germline, I was concerned about the occurence of a “jackpot” event in the male germline,
in which the excision and repair events occur very early on in sperm development resulting in a
clonal expansion of one type of repair event. These events can not be differentiated from
multiple independent excision and repair events of the same type occurring later on in the
spermatogonia. It was necessary to set up as many crosses in vials as possible to obtain 5th
generation female progeny of genotype
𝑤𝑃{𝑤}𝑎
𝑤𝑃( 𝑤) 𝑎
;
+
𝑝𝑖𝑓1𝑝𝑜𝑙32
;
+
+
. So, although there is a small
amount of preliminary data shown in table 1, we know that a majority of yellow-eyed females
have been collected, representing incomplete SDSA. If the control and heterozygous stock were
to produce female progeny that had a majority of red and apricot color (perfect repair or repair
of 9kb through the white gene, respectively) after collecting several hundreds of flies, it would
be safe to postulate that deleting both genes gives female flies even less synthesis in SDSA
excision repair compared to the single mutants. This would agree with the model in which both
PIf1 and Pol32 act in independent pathways.
Conclusion and Future Experiments
In the past, it has been thought that the tranposase used in the assay has an efficiency
of about 20% because the apricot female progeny eye color was assumed to occur via ‘no
excision.’ If the collection of further female progeny shows that the collection of of a majority
of yellow eyed progeny was not a mechanical error, then we may find that the tranposase
efficiency is much higher. So, the next step in my experiment involves the further scoring of

16. 𝑤𝑃{𝑤}𝑎
𝑤𝑃( 𝑤) 𝑎
;
+
𝑝𝑖𝑓1𝑝𝑜𝑙32
;
+
+
flies shown in the 5th generation of figure 1. These females have
incorporated the excision from their father into the germline, but do not contain an active
tranposase. The reason that the color of the female progeny obtained is uniform across the eye,
compared to the 4th generation males, is that one specific excision is contained on the x
chromosome of the female, which does not contain an active transposase in her generation to
excise the element again. Each female can be studied as an independent case of excision repair
in the assay without the tranposase cutting the p element again, as shown in figure 7 below.
Figure 7. The P{w}a consistsof a copiaretrotransposon(apricotcolor) insertedwithinthe whitegene
(redcolor) flankedbylong terminal repeats(black).Thiswholeinsertionresideswithinthe essential
scallopedgene.Whenadouble strandbreakisinduced,precise repairorno excisionwill show a
phenotype of apricoteyes,fullHRwitha total of 9kb of synthesiswillshow redeyes,andabortedHR
and endjoiningwillshowyellow eyes.(Adams, McVey2003)
As this experiment was wholly qualitative analysis with the addition preliminary quantitative
data, we can only suggest that DNA repair in the double mutants may involve decreased

17. synthesis compared to the single mutants of pif1167 and pol32L2 in Drosophila, and that both
genes take part in SDSA. Further analysis of synthesis tract lengths of yellow eyed females is
needed to come to a conclusion. It would be wise to also look at the function of PIF1 and POL32
in telomere maintenance, as the BIR process used as an alternative is likely used in cancerous
cells to maintain growth (Lydeard et al.) Because overproduction of PIF1 is toxic to the cell,
perhaps upregulating PIF1 levels would be a way to combat DNA maintenance in cancerous
cells (Chung).
Works Cited
Adams et al. “Drosophila BLMin Double-Strand Break repair by Synthesis-Dependent Strand
Annealing.” Science 229 (2003): 265-267. Electronic.
Chung, Woo-Hyun. “To Peep into Pif1 Helicase: Multifaceted All the Way from Genome Stability
to Repair-Associated DNA Synthesis.” Journal of Microbiology 52 (2013): 89-95.
Electronic
Kane et al. “Competition between replicative and Tranlesion Polymerases during Homologous
recombination repair in Drosophila.” Plos Genetics 8 (2012): 1-8. Electronic.
Lydeard et al. “Break-induced replication and telomerase-independent telomere maintenance
require Pol32.” Nature 448 (2007): 820-824. Electronic.
McVey et al. “End-Joining Repair of Double-Strand Breaks in Drosophila melanogaster is largely
DNA Ligase IV Independent.” Genetics 168 (2004): 2067-2076. Electronic
Rodger, Kasey. Master’s Thesis 2015