Spotlight

A showcase of research and scholarship

in selected articles from 2014

2014
Editorial Board

CELLULAR GENETICS

Mark Johnston,
Editor-in-Chief
University of Colorado
School of Medicine

Bruce Beutler
The University of Texas
Southwestern Medical
Center

Tracey DePellegrin
Executive Editor

Sue Biggins
Fred Hutchinson Cancer
Research Center

Cristy Gelling
Assistant Editor
Ruth Isaacson
Assistant Managing
Editor
BOARD OF SENIOR
EDITORS

Karen M. Arndt
University of Pittsburgh
Gary A. Churchill
The Jackson
Laboratory
Stanley Fields
University of
Washington
Mark Johnston
University of Colorado
School of Medicine

Orna Cohen-Fix
NIDDK, National
Institutes of Health
Bob Goldstein
University of North
Carolina at Chapel Hill
David I. Greenstein
University of Minnesota
Joseph Heitman
Duke University
Medical Center
Daniel J. Lew
Duke University
Medical Center
Piali Sengupta
Brandeis University
Yongbiao Xue
Chinese Academy of
Sciences

Loeske E. B. Kruuk
University of
Edinburgh
Lauren M. McIntyre
University of Florida
Andrew H. Paterson
University of Georgia
Saunak Sen
University of California,
San Francisco
David W. Threadgill
Texas A&M University

Trudi Schpbach
Princeton University
William T. Sullivan
University of California,
Santa Cruz
Meera V. Sundaram
University of
Pennsylvania
Mariana F. Wolfner
Cornell University
GENE EXPRESSION

Fred van Eeuwijk

Wageningen University

James A. Birchler
University of Missouri

Jason B. Wolf
University of Bath

Michael Freitag
Oregon State
University

Naomi R. Wray
The University of
Queensland
Fei Zou
University of North
Carolina at Chapel Hill

Audrey Gasch
University of
Wisconsin-Madison
Pamela Geyer
University of Iowa

DEVELOPMENTAL
AND BEHAVIORAL
GENETICS

Michael Hampsey
Rutgers Robert Wood
Johnson Medical
School
Alan G. Hinnebusch
NICHD, National
Institutes of Health
Ann Hochschild
Harvard Medical School

COMPLEX TRAITS

Hugo J. Bellen
Baylor College of
Medicine

Terry R. Magnuson
University of North
Carolina at Chapel Hill

Joshua M. Akey
University of
Washington

Kym M. Boycott
CHEO Research
Institute

Michael W. Nachman
University of California,
Berkeley

Justin O. Borevitz
Australian National
University

Lynn Cooley
Yale University

Aaron P. Mitchell
Carnegie Mellon
University

Krista M. Nichols
NOAA Fisheries

Alain Charcosset
Institut National
de la Recherche
Agronomique

Robert J. Duronio
University of North
Carolina at Chapel Hill

Craig S. Pikaard
Indiana University

Charles H. Langley
University of California,
Davis

Mark D. Rose
Princeton University
John C. Schimenti
Cornell University
John Wakeley
Harvard University

Stephen Chenoweth
The University of
Queensland
Dirk Jan de Koning
Swedish University of
Agricultural Sciences
Ina Hoeschele
Virginia Polytechnic
Institute and State
University
Corbin D. Jones
University of North
Carolina at Chapel Hill

David I. Greenstein
University of Minnesota
Marnie E. Halpern
Carnegie Institution for
Science
Iswar K. Hariharan
University of California,
Berkeley
Abraham A. Palmer
University of Chicago
David M. Parichy
University of
Washington
R. Scott Poethig
University of
Pennsylvania

Eric U. Selker
University of Oregon
GENOME INTEGRITY
AND TRANSMISSION

Sharon E. Bickel
Dartmouth College
Monica P. Colaicovo
Harvard Medical School
Nancy M.
Hollingsworth
Stony Brook University
Andreas Houben
Leibniz Institute of
Plant Genetics and
Crop Plant Research

Neil Hunter
University of California,
Davis
James R. Lupski
Baylor College of
Medicine
Jac A. Nickoloff
Colorado State
University
Steven J. Sandler
University of
Massachusetts
Jeff Sekelsky
University of North
Carolina at Chapel Hill
Shyam K. Sharan
NCI, National Institutes
of Health
GENOME AND
SYSTEMS BIOLOGY

Charles Boone
University of Toronto
Stanley Fields
University of
Washington
David A. Largaespada
University of Minnesota
Brian P. Lazzaro
Cornell University
Jeffery F. Miller
University of California,
Los Angeles
Andrew W. Murray
Harvard University
Norbert Perrimon
Harvard Medical School
Enrico G. Petretto
Imperial College
London
Lars M. Steinmetz
European Molecular
Biology Laboratory &
Stanford University
Gary D. Stormo
Washington University
School of Medicine
David Valle
Johns Hopkins
University School of
Medicine
Daniel F. Voytas
University of Minnesota

METHODS,
TECHNOLOGY, AND
RESOURCES

Charles Boone
University of Toronto
Justin O. Borevitz
Australian National
University
George M. Church
Harvard Medical School
Oliver Hobert
Columbia University
Ann Hochschild
Harvard Medical School
Norbert Perrimon
Harvard Medical School
Jeff Sekelsky
University of North
Carolina at Chapel Hill
Jay Shendure
University of
Washington
Gary D. Stormo
Washington University
School of Medicine
David W. Threadgill
Texas A&M University
Daniel F. Voytas
University of Minnesota
STATISTICAL
GENETICS AND
GENOMICS

Ina Hoeschele
Virginia Polytechnic
Institute and State
University
Christina Kendziorski
University of
Wisconsin-Madison
Neil Risch
University of California,
San Francisco
Kathryn M. Roeder
Carnegie Mellon
University
Chiara Sabatti
Stanford University
Saunak Sen
University of California,
San Francisco

Eric A. Stone
North Carolina State
University
Nengjun Yi
University of Alabama
at Birmingham
EMPIRICAL
POPULATION
GENETICS

Daniel A. Barbash
Cornell University
David J. Begun
University of California,
Davis
James J. Bull
University of Texas at
Austin
Deborah Charlesworth
University of
Edinburgh
Anna Di Rienzo
University of Chicago
Santiago C. GonzlezMartnez
Forest Research
Centre (CIFOR-INIA)
Matthew W. Hahn
Indiana University
Lynn B. Jorde
University of Utah
Charles H. Langley
University of California,
Davis
Jeffrey G. Lawrence
University of Pittsburgh
Brian P. Lazzaro
Cornell University
Leonie C. Moyle
Indiana University
Bret A. Payseur
University of
Wisconsin-Madison

THEORETICAL
POPULATION
GENETICS

Nick H. Barton
Institute of Science and
Technology Austria
Mark A. Beaumont
University of Bristol
Joachim Hermisson
University of Vienna
Rasmus Nielsen
University of California,
Berkeley & University
of Copenhagen
Sohini Ramachandran
Brown University
Noah A. Rosenberg
Stanford University
Yun S. Song
University of California,
Berkeley
Wolfgang Stephan
University of Munich
Marcy K. Uyenoyama
Duke University
Lindi M. Wahl
Western University
Jeff D. Wall
University of California,
San Francisco
PRIMERS

Elizabeth A. De Stasio
Lawrence University
PERSPECTIVES

H. Allen Orr
University of Rochester
Adam S. Wilkins
Humboldt University
of Berlin
REVIEWS

Outi Savolainen
University of Oulu

Oliver Hobert
Columbia University

Daniel M. Weinreich
Brown University

Jasper Rine
University of California,
Berkeley

Stephen I. Wright
University of Toronto

Michael Turelli
University of California,
Davis

CRISPRD WORM A Caenorhabditis elegans hermaphrodite glows green

after insertion of GFP in K08F4.2, a gene expressed in the germline and
embryos. A PCR fragment containing GFP flanked by 33-bp homology arms
was used to repair a CRISPR/Cas9 cut near the stop codon of K08F4.2.
See pp 1617 for more 2014 articles describing CRISPR improvements,
innovations, and applications in both model and non-model organisms.
Image courtesy of Alexandre Paix.

Scalable and Versatile Genome Editing Using Linear DNAs with

Microhomology to Cas9 Sites in Caenorhabditis elegans
Alexandre Paix, Yuemeng Wang, Harold E. Smith, Chih-Yung S. Lee,
Deepika Calidas, Tu Lu, Jarrett Smith, Helen Schmidt,
Michael W. Krause, and Geraldine Seydoux
Genetics December 2014 198:13471356

GENETICS: history coupled with vision,

idealism backed by experience.
Thanks to our committed peer editors, peer reviewers,
and authors, GENETICS publishes important advances
across the breadth of genetics and genomics. This
Spotlight showcases the diversity of research and
scholarship we published in 2014.
The coupling of model organism and human genetics
is fast providing a rich understanding of human gene
function, so weve increased our focus on human
genetics. As big data grows even bigger, statistical
genetics is increasingly important, so weve given it its
own section, led by Senior Editor Gary Churchill. And
we added fast-tracked Communications articles for
particularly significant and timely advances.
Were increasing visibility of our authors work,
attracting press coverage from NPRs Science Friday,
NBC and CBS News online, Nature, Science, Science
News, Der Spiegel, Popular Science, Huffington
Post, Christian Science Monitor, The Scientist, and
GenomeWeb, to name a few. And we launched the
GSA Journals blog, Genes to Genomes.
A broad audience reads GENETICS articles and
recognizes their importance. While were more than
a mere metric can capture, annual citations to our
articles are on the rise. Last year was our best yet!
We know you have choices of where to publish. I hope
you will decide it should be with GENETICS, a peeredited journal of the GSA.

Mark Johnston
Editor-in-Chief,
GENETICS

ON THE COVER In 2014, Zimin et al. and Wegrzyn et al. reported the 23-Gb reference
sequence of the loblolly pine, the largest genome sequenced and assembled to date.
Image courtesy of Ron Billings, Texas A&M Forest Service. See Zimin et al. , Genetics
196:875890 and Wegrzyn et al. , Genetics 196:891909.

IN THEIR OWN WORDS

From the day of submission, the editor (Oliver Hobert) handled

everything efficiently and fairly, the paper was sent to review
immediately, the reviews were constructive and helpful, and the
whole process from submission to acceptance took 23 days! Congrats
also to your editorial and production team who put the paper online the
day it was accepted, used social media to broadcast it, accommodated
several revisions, and produced proofs in three weeks. Thank you!
Geraldine Seydoux
Johns Hopkins University School of Medicine

Publishing our epigenetics Perspectives article gave us the

opportunity to clarify our ideas on an important topic and to
reach a reasoned audience. Of all the papers Ive submitted or had
published, I find GENETICS, their editors, and the readers to be the
most willing and agreeable to deep intellectual discussion.
Keith Maggert
Texas A&M University, University of Arizona
Carrie Deans
Texas A&M University

I published a Perspectives asking whether Nobel prize winner Fred

Sanger would get a grant if he applied today. The editorial staff did
a fabulous job highlighting my article, and it quickly rocketed
up in attention on social media. Not using social media myself, I
felt a bit abashed, especially when Nature (media watch) featured the
Perspectives. What was most enjoyable about publishing in GENETICS
was the interaction with the editors, not a compliment I can make about
every journal we publish in. So for good judgment and good publicity,
send your best work to GENETICS.
Stan Fields
Senior Editor, GENETICS, University of Washington

Thank you for providing a fair and competitive platform to publish our
research. I was very pleased with the review process. Our editor Karen
Arndt did an excellent job. Unlike other editors, she read the paper and,
along with the reviewers comments, gave us valuable suggestions on
improving the manuscript. Rarely do we see such detailed reviews these
days. We are very pleased with the end result as the manuscript reads
much better. My experience with other journals is not the same; they
merely send the reviews back with a generic rejection/revisions letter.
Munira Basrai
National Cancer Institute, NIH

CALL FOR PAPERS

Call for Papers: Human Genetics

In its 98-year history, GENETICS has featured many articles about Homo sapiens.
Until recently, however, those papers were largely in the realm of population
genetics. Now, the confluence of model organism and human genetics is
quickly bringing in-depth understanding of human gene function. In fact, because
the depth of human genetic analysis is fast approaching that which is possible
with the experimentally tractable organisms long featured in GENETICS, the
editorial board has signaled its intent to publish more articles identifying human
genes and analyzing their function.
Both GENETICS and G3 are seeking submissions that provide insight into human
gene function and disease, including work that uses model organisms to investigate
the functional effects of candidate disease-associated alleles. More broadly, we
seek to publish research describing methodological and empirical studies of
humans that advance our knowledge of fundamental concepts of genetics.
For more information, see GENETICS Editor-in-Chief Mark Johnstons
October editorial, Humans as a Model Organism: The Time Is Now:
http://www.genetics.org/content/198/2/441.full

Zebrafish models used to investigate a novel ribosomopathy

causing X-linked microcephaly in humans. Image courtesy of
Christelle Golzio, Amalia Kondyles, and Erica Davis.
Brooks and Wall et al. Genetics 198:723733

CELLUL AR GENE TICS

The Anaphase Promoting Complex Regulates

Yeast Lifespan and rDNA Stability by Targeting
Fob1 for Degradation
Johannes Menzel, Mackenzie E. Malo, Cynthia Chan, Martin Prusinkiewicz,
Terra G. Arnason, and Troy A. A. Harkness
Genetics March 2014 196:693709
EDITORS NOTE This article describes a molecular network that monitors
stress, cell cycle progression, protein degradation, genomic stability, and
longevity in yeast. The authors showed that the Anaphase Promoting
Complex (APC) promotes longevity by degradation of Fob1, a protein that
stalls rDNA replication and decreases genomic stability.

ABSTRACT Genomic stability, stress response, and nutrient signaling all play
critical, evolutionarily conserved roles in lifespan determination. However, the
molecular mechanisms coordinating these processes with longevity remain
unresolved. Here we investigate the involvement of the yeast anaphase
promoting complex (APC) in longevity. The APC governs passage through
M and G1 via ubiquitin-dependent targeting of substrate proteins and is
associated with cancer and premature aging when defective. Our two-hybrid
screen utilizing Apc5 as bait recovered the lifespan determinant Fob1 as
prey. Fob1 is unstable specifically in G1, cycles throughout the cell cycle in a
manner similar to Clb2 (an APC target), and is stabilized in APC (apc5CA) and
proteasome (rpn10) mutants. Deletion of FOB1 increased replicative lifespan
(RLS) in wild type (WT), apc5CA, and apc10 cells, and suppressed apc5CA
cell cycle progression and rDNA recombination defects. Alternatively, increased
FOB1 expression decreased RLS in WT cells, but did not reduce the already
short apc5CA RLS, suggesting an epistatic interaction between apc5CA and
fob1. Mutation to a putative L-Box (Fob1E420V), a Destruction Box-like motif,
abolished Fob1 modifications, stabilized the protein, and increased rDNA
recombination. Our work provides a mechanistic role played by the APC to
promote replicative longevity and genomic stability in yeast.

COMPLE X TR AITS

Genetic Variation for Life History Sensitivity

to Seasonal Warming in Arabidopsis thaliana
Yan Li, Riyan Cheng, Kurt A. Spokas, Abraham A. Palmer, and Justin O. Borevitz
Genetics February 2014 196:569577
EDITORS NOTE Climate change is accelerating, altering growing seasons,
and affecting the timing of plant development. This study investigated the
genetic basis of Arabidopsis flowering time under seasonal warming. A
genetic model accurately predicted flowering time of new genotypes in future
conditions, which suggests genomic selection could be used to breed plants
adapted for future environments.

ABSTRACT Climate change has altered life history events in many plant
species; however, little is known about genetic variation underlying seasonal
thermal response. In this study, we simulated current and three future
warming climates and measured flowering time across a globally diverse set
of Arabidopsis thaliana accessions. We found that increased diurnal and
seasonal temperature (13) decreased flowering time in two fall cohorts.
The early fall cohort was unique in that both rapid cycling and overwintering
life history strategies were revealed; the proportion of rapid cycling plants
increased by 37% for each 1 temperature increase. We performed
genome-wide association studies (GWAS) to identify the underlying genetic
basis of thermal sensitivity. GWAS identified five main-effect quantitative
trait loci (QTL) controlling flowering time and another five QTL with thermal
sensitivity. Candidate genes include known flowering loci; a cochaperone that
interacts with heat-shock protein 90; and a flowering hormone, gibberellic
acid, a biosynthetic enzyme. The identified genetic architecture allowed
accurate prediction of flowering phenotypes (R2 > 0.95) that has application
for genomic selection of adaptive genotypes for future environments. This
work may serve as a reference for breeding and conservation genetic studies
under changing environments.

DE VELOPMENTAL & BEHAVIOR AL GENE TICS

A Novel CaM Kinase II Pathway Controls

the Location of Neuropeptide Release from
Caenorhabditis elegans Motor Neurons
Christopher M. Hoover, Stacey L. Edwards, Szi-chieh Yu, Maike Kittelmann,
Janet E. Richmond, Stefan Eimer, Rosalina M. Yorks, and Kenneth G. Miller
Genetics March 2014 196:745765
EDITORS NOTE Neuropeptides are released by exocytosis of storage
compartments called dense core vesicles (DCVs). In neurons, these DCVs
typically travel from the cell soma to the axon before being released. But
what prevents the DCVs taking an early exit on the way to the axon? This
work reports the discovery of a novel CaM Kinase II pathway controlling the
location of DCV exocytosis.

ABSTR ACT Neurons release neuropeptides via the regulated exocytosis

of dense core vesicles (DCVs) to evoke or modulate behaviors. We found
that Caenorhabditis elegans motor neurons send most of their DCVs to
axons, leaving very few in the cell somas. How neurons maintain this skewed
distribution and the extent to which it can be altered to control DCV numbers
in axons or to drive release from somas for different behavioral impacts is
unknown. Using a forward genetic screen, we identified loss-of-function
mutations in UNC-43 (CaM kinase II) that reduce axonal DCV levels by ~90%
and cell soma/dendrite DCV levels by ~80%, leaving small synaptic vesicles
largely unaffected. Blocking regulated secretion in unc-43 mutants restored
near wild-type axonal levels of DCVs. Time-lapse video microscopy showed no
role for CaM kinase II in the transport of DCVs from cell somas to axons. In vivo
secretion assays revealed that much of the missing neuropeptide in unc-43
mutants is secreted via a regulated secretory pathway requiring UNC-31 (CAPS)
and UNC-18 (nSec1). DCV cargo levels in unc-43 mutants are similarly low in
cell somas and the axon initial segment, indicating that the secretion occurs
prior to axonal transport. Genetic pathway analysis suggests that abnormal
neuropeptide function contributes to the sluggish basal locomotion rate of
unc-43 mutants. These results reveal a novel pathway controlling the location
of DCV exocytosis and describe a major new function for CaM kinase II.

COMMENTARY
Dense Core Vesicle Release: Controlling the Where as Well as the When
Stephen Nurrish
Genetics March 2014 196:601-604

GENE E XPRESSION

Additive, Epistatic, and Environmental Effects

Through the Lens of Expression Variability
QTL in a Twin Cohort
Gang Wang, Ence Yang, Candice L. Brinkmeyer-Langford, and James J. Cai
Genetics February 2014 196:413425
EDITORS NOTE Much research has focused on identifying loci that
affect the average value of a phenotype, while ignoring those that affect
the variance, which may also be subject to selection. This work uses data
from a study of more than 300 sets of twins to assess the way genetic and
nongenetic factors contribute to expression variability in humans.

ABSTRACT The expression of a gene can vary across individuals in the

general population, as well as between monozygotic twins. This variable
expression is assumed to be due to the influence of both genetic and
nongenetic factors. Yet little evidence supporting this assumption has been
obtained from empirical data. In this study, we used expression data from
a large twin cohort to investigate the influences of genetic and nongenetic
factors on variable gene expression. We focused on a set of expression
variability QTL (evQTL)i.e., genetic loci associated with the variance, as
opposed to the mean, of gene expression. We identified evQTL for 99, 56,
and 79 genes in lymphoblastoid cell lines, skin, and fat, respectively. The
differences in gene expression, measured by the relative mean difference
(RMD), tended to be larger between pairs of dizygotic (DZ) twins than between
pairs of monozygotic (MZ) twins, showing that genetic background influenced
the expression variability. Furthermore, a more profound RMD was observed
between pairs of MZ twins whose genotypes were associated with greater
expression variability than the RMD found between pairs of MZ twins whose
genotypes were associated with smaller expression variability. This suggests
that nongenetic (e.g., environmental) factors contribute to the variable
expression. Lastly, we demonstrated that the formation of evQTL is likely due
to partial linkages between eQTL SNPs that are additively associated with
the mean of gene expression; in most cases, no epistatic effect is involved.
Our findings have implications for understanding divergent sources of gene
expression variability.

GENE TICS OF SE X

Wild Sex in Zebrafish: Loss of the Natural Sex

Determinant in Domesticated Strains
Catherine A. Wilson, Samantha K. High, Braedan M. McCluskey, Angel Amores,
Yi-lin Yan, Tom A. Titus, Jennifer L. Anderson, Peter Batzel, Michael J. Carvan III,
Manfred Schartl, and John H. Postlethwait
Genetics November 198:12911308
EDITORS NOTE While searching for the elusive sex determination
mechanism of zebrafish, these authors unexpectedly found that domesticated
stocks lack detectable sex-linked loci. This suggests that key components
of the sex determination system were lost during domestication, and variant
mechanisms may have evolved or been unmasked in the lab. This work was
published as part of the GSA journals ongoing Genetics of Sex collection:
http://www.genetics.org/site/misc/GeneticsOfsex.xhtml

ABSTRACT Sex determination can be robustly genetic, strongly environmental,

or genetic subject to environmental perturbation. The genetic basis of
sex determination is unknown for zebrafish (Danio rerio), a model for
development and human health. We used RAD-tag population genomics
to identify sex-linked polymorphisms. After verifying this RAD-sex method
on medaka (Oryzias latipes), we studied two domesticated zebrafish strains
(AB and TU), two natural laboratory strains (WIK and EKW), and two recent
isolates from nature (NA and CB). All four natural strains had a single sexlinked region at the right tip of chromosome 4, enabling sex genotyping
by PCR. Genotypes for the single nucleotide polymorphism (SNP) with the
strongest statistical association to sex suggested that wild zebrafish have
WZ/ZZ sex chromosomes. In natural strains, male genotypes became
males and some female genotypes also became males, suggesting that the
environment or genetic background can cause female-to-male sex reversal.
Surprisingly, TU and AB lacked detectable sex-linked loci. Phylogenomics
rooted on D. nigrofasciatus verified that all strains are monophyletic.
Because AB and TU branched as a monophyletic clade, we could not rule
out shared loss of the wild sex locus in a common ancestor despite their
independent domestication. Mitochondrial DNA sequences showed that
investigated strains represent only one of the three identified zebrafish
haplogroups. Results suggest that zebrafish in nature possess a WZ/ZZ
sex-determination mechanism with a major determinant lying near the right
telomere of chromosome 4 that was modified during domestication. Strains
providing the zebrafish reference genome lack key components of the natural
sex-determination system but may have evolved variant sex-determining
mechanisms during two decades in laboratory culture.

10

GENOME & SYSTEMS BIOLOGY

Systems Genomics of Metabolic Phenotypes

in Wild-Type Drosophila melanogaster
Laura K. Reed, Kevin Lee, Zhi Zhang, Lubna Rashid, Amy Poe, Benjamin Hsieh,
Nigel Deighton, Norm Glassbrook, Rolf Bodmer, and Greg Gibson
Genetics June 197:781793
EDITORS NOTE By dissecting Drosophila transcriptional and metabolic
responses to different diets, the authors showed that genotype-by-diet
interactions are a major component of expression variation, but not of
metabolomic variation. Using evolve-and-resequence experiments to
quantify genomic responses to dietary selection, the authors found rapid
and replicated changes in gene frequency across hundreds of loci.

ABSTRACT Systems biology is an approach to dissection of complex

traits that explicitly recognizes the impact of genetic, physiological, and
environmental interactions in the generation of phenotypic variation.
We describe comprehensive transcriptional and metabolic profiling in
Drosophila melanogaster across four diets, finding little overlap in modular
architecture. Genotype and genotype-by-diet interactions are a major
component of transcriptional variation (24 and 5.3% of the total variation,
respectively) while there were no main effects of diet (<1%). Genotype was
also a major contributor to metabolomic variation (16%), but in contrast to
the transcriptome, diet had a large effect (9%) and the interaction effect
was minor (2%) for the metabolome. Yet specific principal components of
these molecular phenotypes measured in larvae are strongly correlated
with particular metabolic syndrome-like phenotypes such as pupal weight,
larval sugar content and triglyceride content, development time, and cardiac
arrhythmia in adults. The second principal component of the metabolomic
profile is especially informative across these traits with glycine identified as a
key loading variable. To further relate this physiological variability to genotypic
polymorphism, we performed evolve-and-resequence experiments, finding
rapid and replicated changes in gene frequency across hundreds of loci
that are specific to each diet. Adaptation to diet is thus highly polygenic.
However, loci differentially transcribed across diet or previously identified by
RNAi knockdown or expression QTL analysis were not the loci responding to
dietary selection. Therefore, loci that respond to the selective pressures of diet
cannot be readily predicted a priori from functional analyses.

11

GENOME INTEGRIT Y & TR ANSMISSION

Discovery of Supernumerary B Chromosomes

in Drosophila melanogaster
Elisabeth Bauerly, Stacie E. Hughes, Dana R. Vietti, Danny E. Miller, William McDowell,
and R. Scott Hawley
Genetics April 2014 196:10071016
EDITORS NOTE Non-essential extra chromosomes called B chromosomes
have been identified in more than 1300 plant and 500 animal species. This
study identified a lab strain of Drosophila melanogaster that acquired an
average of 10 B chromosomes per fly in just the space of a decade. The
discovery of B chromosomes in a genetically tractable model provides a new
tool for understanding how cells cope with extra chromosomes and how new
chromosomes evolve.

ABSTRACT B chromosomes are small, heterochromatic chromosomes that

are transmitted in a non-Mendelian manner. We have identified a stock of
Drosophila melanogaster that recently (within the last decade) acquired an
average of 10 B chromosomes per fly. These B chromosomes are transmitted
by both males and females and can be maintained for multiple generations
in a wild-type genetic background despite the fact that they cause high levels
of 4th chromosome meiotic nondisjunction in females. Most curiously, these
B chromosomes are mitotically unstable, suggesting either the absence of
critical chromosomal sites or the inability of the meiotic or mitotic systems
to cope with many additional chromosomes. These B chromosomes also
contain centromeres and are primarily composed of the heterochromatic AATAT
satellite sequence. Although the AATAT sequence comprises the majority of
the 4th chromosome heterochromatin, the B chromosomes lack most, if not
all, 4th chromosome euchromatin. Presumably as a consequence of their
heterochromatic content, these B chromosomes significantly modify positioneffect variegation in two separate reporter systems, acting as enhancers of
variegation in one case and suppressors in the other. The identification of B
chromosomes in a genetically tractable organism like D. melanogaster will
facilitate studies of chromosome evolution and the analysis of the mechanisms
by which meiotic and mitotic processes cope with additional chromosomes.

12

IMMUNITY KALEIDOSCOPE Stylized montage of Drosophila larval fat

tissue expressing membrane-associated GFP. The round female gonad is nestled
within the fat tissue. Nuclei are shown in blue. The fat body organ is a major site
of innate immune response to infection. Stronach et al. found that in both fat
body and epithelia, the MAP3K proteins Tak1 and MLK localize to different sites
within the cell, which may contribute to their differential activation by stimuli.
This work was published in the GSA journals ongoing Genetics of Immunity
collection: http://www.genetics.org/site/misc/GeneticsOfImmunity.xhtml
Image courtesy of Beth Stronach.

Domain Specificity of MAP3K Family Members, MLK and Tak1, for

JNK Signaling in Drosophila
Beth Stronach, Ashley L. Lennox, and Rebecca A. Garlena
Genetics 197:497513

13

GENOME INTEGRIT Y & TR ANSMISSION

Evidence for Paternal Age-Related Alterations in

Meiotic Chromosome Dynamics in the Mouse
Lisa A. Vrooman, So I. Nagaoka, Terry J. Hassold, and Patricia A. Hunt
Genetics February 2014 196:385396
EDITORS NOTE Do aging males make poorer quality sperm? In humans,
females over the age of 40 face a well-established risk of producing eggs
with chromosome abnormalities, but it is less clear how age affects meiosis
in males. Vrooman et al. investigated chromosome dynamics during
spermatogenesis in mice. Meiotic errors increased with mouse age, but the
data suggest that aneuploid germ cells were effectively eliminated by cell
cycle checkpoint mechanisms.

ABSTRACT Increasing age in a woman is a well-documented risk factor

for meiotic errors, but the effect of paternal age is less clear. Although it is
generally agreed that spermatogenesis declines with age, the mechanisms
that account for this remain unclear. Because meiosis involves a complex
and tightly regulated series of processes that include DNA replication, DNA
repair, and cell cycle regulation, we postulated that the effects of age might
be evident as an increase in the frequency of meiotic errors. Accordingly, we
analyzed spermatogenesis in male mice of different ages, examining meiotic
chromosome dynamics in spermatocytes at prophase, at metaphase I, and
at metaphase II. Our analyses demonstrate that recombination levels are
reduced in the first wave of spermatogenesis in juvenile mice but increase in
older males. We also observed age-dependent increases in XY chromosome
pairing failure at pachytene and in the frequency of prematurely separated
autosomal homologs at metaphase I. However, we found no evidence of
an age-related increase in aneuploidy at metaphase II, indicating that cells
harboring meiotic errors are eliminated by cycle checkpoint mechanisms,
regardless of paternal age. Taken together, our data suggest that advancing
paternal age affects pairing, synapsis, and recombination between
homologous chromosomesand likely results in reduced sperm counts due
to germ cell lossbut is not an important contributor to aneuploidy.

14

ME THODS, TECHNOLOGY, & RESOURCES

fastSTRUCTURE: Variational Inference of

Population Structure in Large SNP Datasets
Anil Raj, Matthew Stephens, and Jonathan K. Pritchard
Genetics June 2014 197:573589
EDITORS NOTE The STRUCTURE program and its underlying model, first
published 14 years ago in GENETICS, has proven incredibly useful in a wide
range of applications that must account for population structure. However,
the advent of dense SNP arrays has posed severe computational challenges
for the method. This article describes efficient algorithms for approximate
inference of the model underlying STRUCTURE. The new approach,
fastSTRUCTURE, achieves speeds nearly 100 times faster than STRUCTURE,
without compromising accuracy.

ABSTRACT Tools for estimating population structure from genetic data

are now used in a wide variety of applications in population genetics.
However, inferring population structure in large modern data sets imposes
severe computational challenges. Here, we develop efficient algorithms for
approximate inference of the model underlying the STRUCTURE program
using a variational Bayesian framework. Variational methods pose the
problem of computing relevant posterior distributions as an optimization
problem, allowing us to build on recent advances in optimization theory to
develop fast inference tools. In addition, we propose useful heuristic scores
to identify the number of populations represented in a data set and a new
hierarchical prior to detect weak population structure in the data. We test
the variational algorithms on simulated data and illustrate using genotype
data from the CEPHHuman Genome Diversity Panel. The variational
algorithms are almost two orders of magnitude faster than STRUCTURE
and achieve accuracies comparable to those of ADMIXTURE. Furthermore,
our results show that the heuristic scores for choosing model complexity
provide a reasonable range of values for the number of populations
represented in the data, with minimal bias toward detecting structure when
it is very weak. Our algorithm, fastSTRUCTURE, is freely available online at
http://pritchardlab.stanford.edu/structure.html.

COMMENTARY
Variations on a Common STRUCTURE: New Algorithms for a Valuable Model
John Novembre
Genetics July 2014 197:809-811

15

ME THODS, TECHNOLOGY, & RESOURCES: CRISPR

After publishing the first report of CRISPR/Cas9 genome editing in Drosophila

in 2013, GENETICS is already publishing articles describing work in which this
technology is deployed as a routine tool for targeted mutagenesis. In 2014,
GENETICS and G3 also published a series of methodology papers describing
CRISPR improvements, innovations, and applications in both model and nonmodel organisms, including those listed below.
Highly Specific and Efficient CRISPR/Cas9-Catalyzed Homology-Directed Repair
in Drosophila
Scott J. Gratz, Fiona P. Ukken, C. Dustin Rubinstein, Gene Thiede, Laura K. Donohue,
Alexander M. Cummings, and Kate M. OConnor-Giles
Genetics April 2014 196:961971
Efficient Gene Knock-out and Knock-in with Transgenic Cas9 in Drosophila
Zhaoyu Xue, Mengda Ren, Menghua Wu, Junbiao Dai, Yikang S. Rong, and
Guanjun Gao
G3: Genes | Genomes | Genetics May 2014 4:925929
Efficient and Heritable Gene Targeting in Tilapia by CRISPR/Cas9
Minghui Li, Huihui Yang, Jiue Zhao, Lingling Fang, Hongjuan Shi, Mengru Li,
Yunlv Sun, Xianbo Zhang, Dongneng Jiang, Linyan Zhou, and Deshou Wang
Genetics June 2014 197:591599
RNA-Guided Genome Editing in Drosophila with the Purified Cas9 Protein
Jeong-Soo Lee, Su-Jin Kwak, Jungeun Kim, Ae-Kyeong Kim, Hae Min Noh,
Jin-Soo Kim, and Kweon Yu
G3: Genes | Genomes | Genetics July 2014 4:12911295
A Co-CRISPR Strategy for Efficient Genome Editing in Caenorhabditis elegans
Heesun Kim, Takao Ishidate, Krishna S. Ghanta, Meetu Seth, Darryl Conte, Jr.,
Masaki Shirayama, and Craig C. Mello
Genetics August 2014 197:10691080
Performance of the Cas9 Nickase System in Drosophila melanogaster
Xingjie Ren, Zhihao Yang, Decai Mao, Zai Chang, Huan-Huan Qiao, Xia Wang, Jin Sun,
Qun Hu, Yan Cui, Lu-Ping Liu, Jun-Yuan Ji, Jiang Xu, and Jian-Quan Ni
G3: Genes | Genomes | Genetics October 2014 4:19551962
Efficient Marker-Free Recovery of Custom Genetic Modifications with CRISPR/
Cas9 in Caenorhabditis elegans
Joshua A. Arribere, Ryan T. Bell, Becky X. H. Fu, Karen L. Artiles, Phil S. Hartman,
and Andrew Z. Fire
Genetics November 2014 198:837846
CRISPR/Cas9 Mediates Efficient Conditional Mutagenesis in Drosophila
Zhaoyu Xue, Menghua Wu, Kejia Wen, Menda Ren, Li Long, Xuedi Zhang, and
Guanjun Gao
G3: Genes | Genomes | Genetics November 2014 4:21672173

16

Efficient CRISPR/Cas9 Plasmids for Rapid and Versatile Genome Editing

in Drosophila
Joseph Gokcezade, Grzegorz Sienski, and Peter Duchek
G3: Genes | Genomes | Genetics November 2014 4:22792282
Scalable and Versatile Genome Editing Using Linear DNAs with Microhomology
to Cas9 Sites in Caenorhabditis elegans
Alexandre Paix, Yuemeng Wang, Harold E. Smith, Chih-Yung S. Lee, Deepika Calidas,
Tu Lu, Jarrett Smith, Helen Schmidt, Michael W. Krause, and Geraldine Seydoux
Genetics December 2014 198:13471356
RNA-Guided Genome Editing for Target Gene Mutations in Wheat
Santosh Kumar Upadhyay, Jitesh Kumar, Anshu Alok, and Rakesh Tuli
G3: Genes | Genomes | Genetics December 2013 3:22332238
Fast and Efficient Drosophila melanogaster Gene Knock-Ins Using MiMIC
Transposons
Sven Vilain, Roeland Vanhauwaert, Ine Maes, Nils Schoovaerts, Lujia Zhou,
Sandra Soukup, Raquel da Cunha, Elsa Lauwers, Mark Fiers, and Patrik Verstreken
G3: Genes | Genomes | Genetics December 2014 4:23812387
A Versatile Two-Step CRISPR- and RMCE-Based Strategy for Efficient Genome
Engineering in Drosophila
Xu Zhang, Wouter H. Koolhaas, and Frank Schnorrer
G3: Genes | Genomes | Genetics December 2014 4:24092418MTR CRISPR 2

NHGRI-1 is a zebrafish line in which the majority of

polymorphisms have been identified by deep sequencing,
aiding experimental design for sequence-sensitive techniques
like CRISPR/Cas9 applications.
Image courtesy of Darryl Leja and Julia Fekecs.
LaFave et al. Genetics 198:167170

17

PERSPECTIVES

The Domestication Syndrome in Mammals:

A Unified Explanation Based on Neural Crest
Cell Behavior and Genetics
Adam S. Wilkins, Richard W. Wrangham, and W. Tecumseh Fitch
Genetics July 2014 197:795-808
EDITORS NOTE More than 140 years ago, Darwin noticed something
peculiar about domesticated mammals. Besides being tamer than their
wild ancestors, domestic species tend to have floppier ears, patches of
white fur, and more juvenile faces with smaller jaws, among other traits. In
this Perspectives article, the authors proposed an intriguing hypothesis to
explain domestication syndrome, a proposal that continues to generate
considerable commentary, discussion, and press coverage.

ABSTRACT Charles Darwin, while trying to devise a general theory of

heredity from the observations of animal and plant breeders, discovered that
domesticated mammals possess a distinctive and unusual suite of heritable
traits not seen in their wild progenitors. Some of these traits also appear in
domesticated birds and fish. The origin of Darwins domestication syndrome
has remained a conundrum for more than 140 years. Most explanations
focus on particular traits, while neglecting others, or on the possible selective
factors involved in domestication rather than the underlying developmental
and genetic causes of these traits. Here, we propose that the domestication
syndrome results predominantly from mild neural crest cell deficits during
embryonic development. Most of the modified traits, both morphological
and physiological, can be readily explained as direct consequences of such
deficiencies, while other traits are explicable as indirect consequences.
We first show how the hypothesis can account for the multiple, apparently
unrelated traits of the syndrome and then explore its genetic dimensions and
predictions, reviewing the available genetic evidence. The article concludes
with a brief discussion of some genetic and developmental questions raised
by the idea, along with specific predictions and experimental tests.

18

DOMESTICATION SYNDROME Alexander Cagan, PhD student at the

Max Planck Institute for Evolutionary Anthropology, studies the genetics
of domestication and creates unique drawings that summarize conference
talks and research abstracts. This noteworthy image shows Cagans take on
the Wilkins et al. domestication syndrome hypothesis. The images represent
(counterclockwise, from top left): Domesticated mammals; a domesticated
fox with the traits of domestication syndrome (weakened ear cartilage/floppy
ears, shortened snouts, reduced tooth size, melanocyte/pigmentation changes,
and reduced brain size); the phenomenon of pleiotropy, in which seemingly
unrelated traits are linked by variation at one or a small number of genes; the
neural crest cell distribution in a mammalian embryo; systems affected by
neural tube development (including sympathetic ganglia, adrenals, and tail
cartilage); a dog skull showing reduced jaw size. See more of Cagans work at
his Twitter feed: https://twitter.com/ATJCagan

19

POPUL ATION & E VOLUTIONARY GENE TICS

Stability and Response of Polygenic Traits to

Stabilizing Selection and Mutation
Harold P. de Vladar and Nick Barton
Genetics June 2014 197:749767
EDITORS NOTE Stabilizing selection seems to affect most traits. This work
showed that stabilizing selection leads to a sharp threshold separating large
and small allelic effects. Quantitative variation is due mostly to alleles of large
effect, which remain near fixation. In contrast to models that assume equal
allelic effects, these results show that traits under mutation-selection balance
are expected to be well adapted and do not become trapped at suboptimal
fitness peaks.

ABSTRACT When polygenic traits are under stabilizing selection, many

different combinations of alleles allow close adaptation to the optimum. If alleles
have equal effects, all combinations that result in the same deviation from the
optimum are equivalent. Furthermore, the genetic variance that is maintained
by mutationselection balance is 2/S per locus, where is the mutation rate
and S the strength of stabilizing selection. In reality, alleles vary in their effects,
making the fitness landscape asymmetric and complicating analysis of the
equilibria. We show that that the resulting genetic variance depends on the
fraction of alleles near fixation, which contribute by 2/S, and on the total
mutational effects of alleles that are at intermediate frequency. The interplay
between stabilizing selection and mutation leads to a sharp transition: alleles
with effects smaller than a threshold value of 2 /S remain polymorphic,
whereas those with larger effects are fixed. The genetic load in equilibrium is
less than for traits of equal effects, and the fitness equilibria are more similar.
We find that if the optimum is displaced, alleles with effects close to the
threshold value sweep first, and their rate of increase is bounded by S. Longterm response leads in general to well-adapted traits, unlike the case of equal
effects that often end up at a suboptimal fitness peak. However, the particular
peaks to which the populations converge are extremely sensitive to the initial
states and to the speed of the shift of the optimum trait value.

20

DISSECTING COMPLEXITY Variation in colony shape, a complex

trait, among a family of budding yeast strains. Many methods have been
developed for identifying quantitative trait loci underlying such phenotypes,
but narrowing candidate regions to single genes and detecting interactions
both remain a challenge. Wilkening, Lin, and Fritsch et al. comprehensively
evaluated three powerful high-throughput approaches to QTL mapping
in yeast, dissecting performance differences and confounding factors, and
examining the contribution of interactions. The image shows a false-colored
subset of 768 meiotic segregants derived from a cross between one strain with
smooth colonies and another with wrinkled colonies.
Image courtesy of Petra Riedinger / Stefan Wilkening / Steinmetz lab.

An Evaluation of High-Throughput Approaches to QTL Mapping in

Saccharomyces cerevisiae
Stefan Wilkening, Gen Lin, Emilie S. Fritsch, Manu M. Tekkedil,
Simon Anders, Raquel Kuehn, Michelle Nguyen, Raeka S. Aiyar,
Michael Proctor, Nikita A. Sakhanenko, David J. Galas, Julien Gagneur,
Adam Deutschbauer, and Lars M. Steinmetz
Genetics March 2014 196:853865

21

POPUL ATION & E VOLUTIONARY GENE TICS

The Fates of Mutant Lineages

and the Distribution of Fitness Effects
of Beneficial Mutations in Laboratory
Budding Yeast Populations
Evgeni M. Frenkel, Benjamin H. Good, and Michael M. Desai
Genetics April 2014 196:1217-1226
EDITORS NOTE The fate of a beneficial mutation depends on both luck
and merit. Even when carried by many individuals, a beneficial mutation may
be driven to extinction by competition from fitter mutations spreading through
the population. The authors examined this process in lab-evolved yeast
populations to understand which mutations can decisively overcome this
competition and how often they occur.

ABSTRACT The outcomes of evolution are determined by which mutations

occur and fix. In rapidly adapting microbial populations, this process
is particularly hard to predict because lineages with different beneficial
mutations often spread simultaneously and interfere with one anothers
fixation. Hence to predict the fate of any individual variant, we must know the
rate at which new mutations create competing lineages of higher fitness. Here,
we directly measured the effect of this interference on the fates of specific
adaptive variants in laboratory Saccharomyces cerevisiae populations and
used these measurements to infer the distribution of fitness effects of new
beneficial mutations. To do so, we seeded marked lineages with different
fitness advantages into replicate populations and tracked their subsequent
frequencies for hundreds of generations. Our results illustrate the transition
between strongly advantageous lineages that decisively sweep to fixation
and more moderately advantageous lineages that are often outcompeted by
new mutations arising during the course of the experiment. We developed
an approximate likelihood framework to compare our data to simulations
and found that the effects of these competing beneficial mutations were best
approximated by an exponential distribution, rather than one with a single
effect size. We then used this inferred distribution of fitness effects to predict
the rate of adaptation in a set of independent control populations. Finally, we
discuss how our experimental design can serve as a screen for rare, largeeffect beneficial mutations.

22

NEW MOON The bristle worm Platynereis dumerilii has a long history as a
model for circalunar chronobiology and has proven an important reference
species for evolution and development studies. A pair of articles published in
2014 marks a new phase for the bristle worm as a tractable molecular genetic
model. Bannister et al. describe the first method for generating targeted genome
modifications in annelids, while Zantke and Bannister et al. review the wealth of
recently established Platynereis experimental tools. The artwork here represents
the transformation of the living fossil to a functional laboratory model.
Image courtesy of Florian Raible.

TALENs Mediate Efficient and Heritable Mutation of Endogenous

Genes in the Marine Annelid Platynereis dumerilii
Stephanie Bannister, Olga Antonova, Alessandra Polo,
Claudia Lohs, Natalia Hallay, Agne Valinciute, Florian Raible, and
Kristin Tessmar-Raible
Genetics May 2014 197:7789
Genetic and Genomic Tools for the Marine Annelid Platynereis dumerilii
Juliane Zantke, Stephanie Bannister, Vinoth Babu Veedin Rajan,
Florian Raible, and Kristin Tessmar-Raible
Genetics May 2014 197:1931

23

PRIMERS

Budding Yeast for Budding Geneticists:

A Primer on the Saccharomyces cerevisiae
Model System
Andrea A. Duina, Mary E. Miller, and Jill B. Keeney
Genetics May 2014 197:3348
EDITORS NOTE Primers are designed to help both educators and students
in the classroom. Many Primers relate to a current article in GENETICS, making
the article more accessible by offering background and a guide for the nonspecialist reader. In 2014, GENETICS published Primers on articles related
to gene expression, evolutionary genetics, and development, along with the
inaugural Model Organism Primer, introducing readers to the methods and
impact of the widely used eukaryotic cell model S. cerevisiae.

ABSTRACT The budding yeast Saccharomyces cerevisiae is a powerful

model organism for studying fundamental aspects of eukaryotic cell biology.
This Primer article presents a brief historical perspective on the emergence
of this organism as a premier experimental system over the course of the
past century. An overview of the central features of the S. cerevisiae genome,
including the nature of its genetic elements and general organization, is also
provided. Some of the most common experimental tools and resources
available to yeast geneticists are presented in a way designed to engage and
challenge undergraduate and graduate students eager to learn more about the
experimental amenability of budding yeast. Finally, a discussion of several major
discoveries derived from yeast studies highlights the far-reaching impact that
the yeast system has had and will continue to have on our understanding of a
variety of cellular processes relevant to all eukaryotes, including humans.

24

STATISTICAL GENE TICS & GENOMICS

Identifying Causal Variants at Loci with

Multiple Signals of Association
Farhad Hormozdiari, Emrah Kostem, Eun Yong Kang, Bogdan Pasaniuc, and Eleazar Eskin
Genetics October 2014 198:497508
EDITORS NOTE Only a handful of causal variants have been found from the
thousands of risk loci identified in genome-wide association studies. Previous
methods for predicting which variants are causal assumed that only a single
such variant exists for each risk locus. In this work, the authors proposed an
alternative framework that allows for an arbitrary number of causal variants,
and outperforms other methods.

ABSTRACT Although genome-wide association studies have successfully

identified thousands of risk loci for complex traits, only a handful of the
biologically causal variants, responsible for association at these loci, have
been successfully identified. Current statistical methods for identifying
causal variants at risk loci either use the strength of the association signal
in an iterative conditioning framework or estimate probabilities for variants
to be causal. A main drawback of existing methods is that they rely on the
simplifying assumption of a single causal variant at each risk locus, which is
typically invalid at many risk loci. In this work, we propose a new statistical
framework that allows for the possibility of an arbitrary number of causal
variants when estimating the posterior probability of a variant being causal.
A direct benefit of our approach is that we predict a set of variants for each
locus that under reasonable assumptions will contain all of the true causal
variants with a high confidence level (e.g., 95%) even when the locus contains
multiple causal variants. We use simulations to show that our approach
provides 2050% improvement in our ability to identify the causal variants
compared to the existing methods at loci harboring multiple causal variants.
We validate our approach using empirical data from an expression QTL study
of CHI3L2 to identify new causal variants that affect gene expression at this
locus. CAVIAR is publicly available online at http://genetics.cs.ucla.edu/caviar/.

25

Why publish in GENETICS & G3?

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Tired of reformatting manuscripts? We welcome initial submissions in any format
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Your manuscripts will be handled by practicing scientists like you, who understand
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Decision letter parses reviews to offer specific
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Sister Journals, One-Touch Transfer

If you submit a manuscript to GENETICS that reports high-quality and
useful findingsbut lacks the broad appeal, significance, or novelty of
a published GENETICS articleyou may be offered a transfer to G3.
This seamless process either guarantees review at G3, or G3 editors
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