Biology Reference
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interactions in an appropriately matched GWAS context may
be a fruitful approach, particularly as reverse genetic screens
become more scalable in complex eukaryotes, including
human cell lines.
[15] Bender A, Pringle JR. Use of a screen for synthetic lethal and
multicopy suppressor mutants to identify two new genes involved
in morphogenesis in Saccharomyces cerevisiae. Mol Cell Biol
1991;11:1295
305.
[16] Boone C, Bussey H, Andrews BJ. Exploring genetic interactions
and networks with yeast. Nat Rev Genet 2007;8:437 e 49.
[17] Baryshnikova A, et al. Quantitative analysis of fitness and genetic
interactions in yeast on a genome-wide scale. Nat Methods
2010;7:1017 e 24.
[18] Bandyopadhyay S, Kelley R, Krogan NJ, Ideker T. Functional
maps of protein complexes from quantitative genetic interaction
data. PLoS Comput Biol 2008;4:e1000065.
[19] St. Onge RP, et al. Systematic pathway analysis using high-
resolution fitness profiling of combinatorial gene deletions. Nat
Genet 2007;39:199 e 206.
[20] Drees BL, et al. Derivation of genetic interaction networks from
quantitative phenotype data. Genome Biology 2005;6:R38.
[21] Breslow DK, et al. A comprehensive strategy enabling high-
resolution functional analysis of the yeast genome. Nat Methods
2008;5:711 e 8.
[22] Davierwala AP, et al. The synthetic genetic interaction spectrum
of essential genes. Nat Genet 2005;37:1147 e 52.
[23] Zuk O, Hechter E, Sunyaev SR, Lander ES. The mystery of
missing heritability: Genetic interactions create phantom herita-
bility. P Natl Acad Sci USA 2012;109:1193.
[24] Pan X, et al. A robust toolkit for functional profiling of the yeast
genome. Mol Cell 2004;16:487
e
ACKNOWLEDGEMENTS
CB, CLM and BA are supported by a grant from the National Institutes
of Health (1R01HG005853). CB and BA are supported by grants from
the Canadian Institutes of Health Research (MOP-102629)(MOP-
97939) and the Ontario Research Fund (GL2-01-22). CB is supported
by grants from the Canadian Institutes of Health Research (MOP-
57830) and the Natural Sciences and Engineering Council of Canada
(RGPIN 204899-06). BA is supported by a grant from the Canadian
Institutes of Health Research (MOP-11206). CLM is supported by
grants from the National Institutes of Health (1R01HG005084-01A1)
and the National Science Foundation (DBI 0953881). CLM is partially
supported by funding from the University of Minnesota Biomedical
Informatics and Computational Biology program, and a seed grant
from the Minnesota Supercomputing Institute.
REFERENCES
[1] Waddington CH. The Strategy of the Gene. Allen and Unwin,
London 1957.
[2] Costanzo M, et al. The genetic landscape of a cell. Science
2010;327:425
31.
[3] Tong AH, et al. Global mapping of the yeast genetic interaction
network. Science 2004;303:808
96.
[25] Pan X, et al. A DNA integrity network in the yeast Saccharomyces
cerevisiae. Cell 2006;124:1069 e 81.
[26] Lin YY, et al. Protein acetylation microarray reveals that NuA4
controls key metabolic target regulating gluconeogenesis. Cell
2009;136:1073 e 84.
[27] Decourty L, et al. Linking functionally related genes by sensitive
and quantitative characterization of genetic interaction profiles.
Proc Natl Acad Sci U S A 2008;105:5821.
[28] DeLuna A, et al. Exposing the fitness contribution of duplicated
genes. Nat Genet 2008;40:676 e 81.
[29] Costanzo M, Baryshnikova A, Myers CL, Andrews B, Boone C.
Charting the genetic interaction map of a cell. Curr Opin Bio-
technol 2011;22:66 e 74.
[30] Collins SR, Schuldiner M, Krogan NJ, Weissman JS. A strategy
for extracting and analyzing large-scale quantitative epistatic
interaction data. Genome Biol 2006;7:R63.
[31] Eisen MB, Spellman PT, Brown PO, Botstein D. Cluster analysis
and display of genome-wide expression patterns. Proc Natl Acad
Sci U S A 1998;95:14863.
[32] Segre D, Deluna A, Church GM, Kishony R. Modular epistasis in
yeast metabolism. Nat Genet 2005;37:77
e
e
13.
[4] Tong AH, et al. Systematic genetic analysis with ordered arrays of
yeast deletion mutants. Science 2001;294:2364 e 8.
[5] Giaever G, et al. Functional profiling of the Saccharomyces cer-
evisiae genome. Nature 2002;418:387 e 91.
[6] Winzeler EA, et al. Functional characterization of the S. cer-
evisiae genome by gene deletion and parallel analysis. Science
1999;285:901 e 6.
[7] Hartman JLt, Garvik B, Hartwell L, Principles for the buffering of
genetic variation. Science 2001;291:1001 e 4.
[8] Bateson W. Mendel's Priciples of Heredity. Cambridge University
Press, Cambridge;1909.
[9] Fisher RA. The correlation between relatives on the supposition
of Mendelian inheritance. Proc R Soc Edinburgh 1918;52:
399 e 433.
[10] Phillips PC, Otto SP, Whitlock MC. Beyond the average: the
evolutionary importance of gene interactions and variability of
epistatic effects. In: Wolf JB, Brodie ED, Wade MJ, editors.
Epistasis and the Evolutionary Process. New York: Oxford
University Press Inc.; 2000. p. 20 e 40.
[11] Mani R, St Onge RP. J.L. t. Hartman, G. Giaever, F.P. Roth, Defining
genetic interaction. Proc Natl Acad Sci U S A 2008;105:3461 e 6.
[12] Dobzhansky T. Genetics of natural poulations. Xiii. Recombina-
tion and variability in populations of Drosophila pseudoobscura.
Genetics 1946;31:269
e
83.
[33] Leidel S, et al. Ubiquitin-related modifier Urm1 acts as a sulphur
carrier in thiolation of eukaryotic transfer RNA. Nature 2009;
458:228
e
32.
[34] Kelley R, Ideker T. Systematic interpretation of genetic
interactions using protein networks. Nat Biotechnol 2005;23:
561 e 6.
[35] Ulitsky I, Shlomi T, Kupiec M, Shamir R. From E-MAPs to
module maps: dissecting quantitative genetic interactions using
physical interactions. Mol Syst Biol 2008;4:209.
e
90.
[13] Novick P, Botstein D. Phenotypic analysis of temperature-sensi-
tive yeast actin mutants. Cell 1985;40:405
e
16.
[14] Guarente L. Synthetic enhancement in gene interaction: a genetic
tool come of age. Trends Genet 1993;9:362.
e
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