Finally we also published a paper in Transfusion last year with more detailed comparison of whole genome sequencing and blood group serology for 24 antigens: onlinelibrary.wiley.com/doi/10.1111/... 12/12
Nonetheless, it is protective against this infection and so could have contributed to a historically lower P. vivax prevalence in the southern Arabian peninsula than nearby countries with lower Duffy null allele frequency. 11/n
Duffy negativity is associated with neutropenia and potentially other phenotypes and so we question whether P. vivax malaria is truly the driving selective pressure across such different environmental contexts... 10/n
Finally, we reflected on the multiple, consistent findings of strong selection for this allele in different African-admixed populations that others have reported (e.g., Cape Verde, Madagascar, Pakistan, Sudan). 9/n
We think this makes sense – as soon as the Duffy negative allele was introduced, it appears to have spread. We did not see any signal of enrichment for African ancestry surrounding loci that have been associated with protection from P. falciparum malaria. 8/n
Oman has a long history of interaction with East Africa, and we inferred a two-pulse model of admixture, 5 and 59 generations ago. The haplotypes surrounding the Duffy negative allele are short – much more consistent with an older introduction. 7/n
Mostly this was due to the same RBC-specific enhancer mutation that is common across Africa, and the locus had a strong increase in local African ancestry to 78% (vs. 11% genome-wide). We also found a null frameshift allele that contributes to Duffy negativity specifically in the Middle East. 6/n
With funding from the Omani Research Council (and later NIH to my group), we performed paired blood group serology and whole genome sequencing. Indeed, we confirmed that absence of Duffy antigen was very common, with 87/100 lacking this important receptor for P. vivax on their RBCs. 5/n
We wondered how admixture and selective pressure from malaria played a role. Some blood group alleles are associated with protection from P. vivax malaria, others with P. falciparum malaria, both of which have been present in Oman (though it is now malaria-free). 4/n
Arwa noted that in her studies of blood group antigens in Oman, some had more similar frequencies to African populations and some to European populations. 3/n
We report analyses of whole genome sequence data from 100 Omani blood donors. This project stemmed from a conversation with Dr. Arwa Al-Riyami, a hematologist at Sultan Qaboos University in Muscat, at the International Society for Blood Transfusion meeting in Toronto in 2018. 2/n
So pleased to share that our paper (led by Paige Haffener and in collaboration with @drriyamia.bsky.social) on genomic variation in Oman is now published in AJHG! www.cell.com/ajhg/fulltex... 1/n
We've launched a department Trainee Emergency Fund, to help support EVERYONE BELONGING IN SCIENCE by meeting urgent financial needs of students and postdocs. Every gift will be matched, up to $1,000, by Nels Elde. Click to see a message from Aaron Quinlan and to donate!
www.givecampus.com/s/w46xg1
I am hiring a staff bioinformatician for my new lab at the University of Utah! Please consider applying if you are on the hunt:
employment.utah.edu/salt-lake-ci...
Come be our colleague! The University of Rochester is hiring a TT Assistant Professor in evolutionary genetics and genomics: apply.interfolio.com/173431.
Thanks to a constructive peer review, the published paper in PLoS Pathogens is stronger than the preprint, so thanks to the editor and reviewers!
We also identify genes with high SNP density, including genes in the Hep1 and Hep2 gene families, which are unique to Hepatocystis. This might suggest they are under selection for immune evasion, despite Hepatocystis lacking blood stage replication.
This gave us low-coverage whole-genome sequencing data for Hepatocystis from baboons and five species of Chlorocebus monkeys-- and so a first look at genetic variation and population structure genome-wide. There is support for substructure by host species, which was not as clear from mtDNA only.
Congrats to the lab! We were parasites of parasite data, and recovered DNA sequences from Hepatocystis (a close relative of human malaria parasites) from 37 wild non-human primates originally sequenced to look at the host genome, whose blood happened to be sampled while infected. shorturl.at/KluV8
Thanks to a constructive peer review, the published paper in PLoS Pathogens is stronger than the preprint, so thanks to the editor and reviewers!
We also identify genes with high SNP density, including genes in the Hep1 and Hep2 gene familiels, which are unique to Hepatocystis. This might suggest they are under selection for immune evasion, despite Hepatocystis lacking blood stage replication
This gave us low-coverage whole-genome sequencing data for Hepatocystis from baboons and five species of Chlorocebus monkeys-- and so a first look at genetic variation and population structure genome-wide. There is support for substructure by host species, which was not as clear from mtDNA only.
Welcome!!!
Postdocs: Human Genetics at Utah will be hosting our annual Rising Stars in Genetics and Genomics Symposium in Sept. Apply here: shorturl.at/wBMg2
There will be sessions on developmental, evolutionary and disease genetics. A chance be invited to SLC to network here and with peers! Please share.
Quantgen GRC (16-21 Feb 2025) updates: we are now 75% subscribed!
Deadline: 19 Jan 2025
BUT: We will pick talks from submitted abstracts 16 Dec and aim to send decisions before Xmas. So submit your abstracts now (even if not perfect - editable after submission)!
www.grc.org/quantitative...
Recently learned about preLights -- and happy to support Alejandra (postdoc in the lab) as a contributor to highlight and generate discussion around preprints in evolutionary biology!
t.co/oaiz287N4a