Genetics Society of America
GSA connects you to the field through a range of scholarly and community publications: our peer-reviewed journals offer two distinct platforms for communicating high-quality original research; our blog brings perspective to your research and career; and our newsletters keep you up to date with the latest opportunities and news from your community.
GENETICS publishes high-quality genetics and genomics research that expands scientific boundaries—we’ve been building the field since 1916. With its broad readership, rich history, and responsive editors, GENETICS brings the latest in publishing innovations to the communities it serves. We invite you to submit your research and discover the fast turnaround times and helpful review process for yourself.
Get your useful data out into the world by publishing in G3: Genes|Genomes|Genetics. G3 publishes high quality foundational research, particularly studies that generate useful genetic information, such as mutant screens, single gene studies, genome maps, genome sequence data, GWAS and QTL studies, software, data resources, and new methods. The Editorial Board of G3 believes that rapid dissemination of such data lays the foundation for many important insights.
We treat authors as colleagues, not adversaries. Your time is important—and so is your research. Peer editors oversee the review process and give you clear guidance on how to address any reviewer comments; our helpful editorial staff keep the process moving and on time. We make it easy to submit: no formatting requirements on initial submission. Our dedicated editors work hard to keep time to first decision at around a month. And because we’re agile and community-driven, we’ve long been at the forefront of publishing innovations.
The GSA Journals are committed to helping authors get their work in front a wide audience. Our Promotional Toolkit for Authors contains pointers to help you promote your GENETICS or G3: Genes|Genomes|Genetics paper, including how GSA and Oxford University Press can help.
The review experience has been the single most useful and pleasant of my career. The reviews were constructive and fair, the editor provided exceptionally clear guidance, and turn-around on the revision was lightning fast.
Genes to Genomes, the GSA blog, features news from the GSA community, highlights from the GSA journals, and posts from staff and guest authors about careers, professional development, science policy, publishing, education, outreach, equity and inclusion, and the intersections of science, art, and culture. Propose a guest post yourself and start a conversation!
In March 2016, GENETICS launched WormBook, a comprehensive compendium of review articles presenting the current state of knowledge in C. elegans research. WormBook articles span the breadth of the biology, genetics, genomics, and evolutionary biology of C. elegans. Find historical WormBook articles published as the online companion to WormBase here. This page contains the full list of all historical and GSA-published WormBook articles, organized by section.
Characterizing how mutations bring about phenotypic changes is a common strategy for identifying molecular underpinnings. A perspective article in GENETICS challenges the way researchers categorize mutations as gain-of-function and advises how to avoid misleading labeling.
AbstractBiofilm formation is vital for survival and pathogenicity of the fungus Candida albicans. Expression of biofilm-promoting genes is coordinated by a transcription factor network that governs the yeast-filament transition and other processes. A second cell type transition, the white-opaque transition, is coordinated by its own transcription factor network. Initial studies suggested that the two transcriptional networks have a mutually exclusive relationship, driven in part by reciprocal repression of biofilm regulator Efg1 and white-opaque regulator Wor1....
AbstractThe nervous system is highly sensitive to alterations in the dosage of genes crucial for neurodevelopment, as exemplified by retinoic acid-induced 1 (RAI1). A 50% change in RAI1 gene copy number, resulting in either reduced or increased protein levels, leads to distinct neurodevelopmental disorders. RAI1 haploinsufficiency causes Smith–Magenis syndrome (SMS), whereas RAI1 duplication underlies Potocki–Lupski syndrome (PTLS). We recently demonstrated that restoring Rai1 levels can improve SMS-related disease phenotypes in mice. However, despite protein stability...
