A su-cute-lent rodent

The cactus mouse (Peromyscus eremicus) is a small desert-adapted rodent living in the deserts of the North America southwest. Its desert adaptations are so extreme that it can stop producing urine to conserve water and show minimal signs of physiological stress. If you were exposed to the conditions the cactus mouse is usually exposed to, both in terms of high temperature and dehydration, you will die pretty soon, surely in less than 3 days. These cactus mice thrive under these extreme conditions instead!

Cactus mouse, photo by Anna Tigano

In the MacManes Lab at the University of New Hampshire (USA), we study the genomic and physiological basis of the cactus mouse desert adaptations. Not only is the cactus mouse a very evolutionarily and physiologically interesting species, but it also is amenable to life in captivity. Taken together, this makes the species an ideal candidate to combine lab experiments and field work to understand what traits make it so well fit to life in the desert and the genomic and physiological basis of these traits.

Recently, we produced a chromosome-level assembly of the cactus mouse genome to enable population, comparative and functional genomics analyses to identify genes associated with adaptation (including to deserts) and speciation in this and other species (Tigano et al. 2020; plus a lot of more work currently in progress). As we assembled more Peromyscus genomes in collaboration with DNA Zoo (e.g., Peromyscus crinitus and P. nasutus) we realized that the cactus mouse genome presented a few assembly errors. So today, we are happy to share the 2.0.0 version of the cactus mouse genome assembly, corrected and reordered using the Hi-C data generated using the T.C. Hsu Cryo-Zoo at the University of Texas MD Anderson Cancer Center cell line collection. This new corrected assembly is timely as we start to look in the chromosomal rearrangements that are associated with adaptation and speciation in Peromyscus mice.

This assembly has a contig N50 = 20Kb and a scaffold N50 = 122Mb.

MacManes Lab https://macmanes.weebly.com/

Tigano A, Colella JP, MacManes MD. 2020. Comparative and population genomics approaches reveal the basis of adaptation to deserts in a small rodent. Molecular Ecology, 29(7), 1300-1314. https://onlinelibrary.wiley.com/doi/full/10.1111/mec.15401

Earn your stripes!

Grant’s zebra (Equus quagga boehmi) is the smallest of the seven subspecies of the plains zebra (Equus quagga) aka the common zebra. In Africa, Grant’s zebras roam grasslands and savannahs, eating coarse grasses that other grazing animals may not ingest. Though there are more wild populations of Grant’s zebra than other zebra species, they are not immune to environmental threats. The IUCN categorizes Grant’s zebra as near threatened with its population in decline, mostly due to habitat loss for agricultural development and human conflicts in their regions.

Mother and foal, photo by Seth Eisenberg [CC BY-SA 4.0], via wikimedia.org

Of course, zebras are famous for their contrasting black and white stripes. Incredibly, there is still ongoing debate about why they sport their unusual striped pattern. Many functions have been proposed, including camouflage, repelling insects and thermoregulation [1,2,3].

Among some of the more recent findings on the matter of zebra striping is the correlation between the intensity and opacity of striping in zebras and their native environment’s temperature. Generally, zebra species that inhabit warmer climates have dark, broad stripes that cover most of their body. In the cooler regions near South Africa, the striping pattern is lighter, thinner, and may only cover the head and abdomen. Based on this finding, researches can now accurately predict what the zebras in different regions of Africa look like! Read more about this here.

The debate on how the zebra got its stripes goes all the way back to Charles Darwin and Alfred Russel Wallace. To bring in some genomics resources to weigh in on the question, we release today a de novo chromosome-length genome assembly for the Grant’s zebra. This is a $1K genome assembly with contig N50 = 89kb and scaffold N50 = 114Mb. This assembly was created with the help of two zebras: Ziggy from the Houston Zoo and Zena from Hearts and Hands Animal Rescue. Thank you, Nancy Nunke (Hearts and Hands Animal Rescue), Greg Barsh (Stanford University/Hudson Alpha) and Brenda Larison (UCLA) for their help with this assembly! Follow this link to visit the assembly page.

See below how the Grant zebra’s chromosomes relate to those of a domestic horse. That’s a lot of rearrangements for only ~4 million years separating the species! (Compare this, for example, to the very stable chromosomes in the cat family.)

Whole-genome alignment of the Grant’s zebra assembly (Equus_quagga_boehmi) to the domestic horse (EquCab2.0).

Post by: Ruqayya Khan, Olga Dudchenko

P.S.: If you have ever wondered if the zebras are black with white stripes or white with black stripes, wonder no more; the questions has finally been definitively answered!

P.P.S.: Since Grant's derives from a subspecies designation and subspecific designations are somewhat dubious, on the assembly page we refer to the species as plains zebra.

A Parasitic flatworm infecting over 15 million with no vaccine

Parasitic flatworms cause substantial death and disease in humans. The Chinese liver fluke, Clonorchis sinensis, is one of the most destructive parasitic worms in humans in China, Vietnam, Korea and the Russian Far East. Read more about Chinese liver flukes on Wikipedia.

Banchob Sripa, Sasithorn Kaewkes, Paiboon Sithithaworn, Eimorn Mairiang, Thewarach Laha, Michael Smout, Chawalit Pairojkul, Vajaraphongsa Bhudhisawasdi, Smarn Tesana, Bandit Thinkamrop, Jeffrey M. Bethony, Alex Loukas & Paul J. Brindley / CC BY (https://creativecommons.org/licenses/by/2.5)

Although C. sinensis infection can be controlled relatively well using drugs (anthelmintics), the worm can cause cancer (cholangiocarcinoma) and causes major suffering in ~ 15 million people infected in Asia. No vaccine is available to prevent parasite infection, and humans have no resistance to reinfection.

To better control this flatworm, research has been conducted on the molecular biology of the parasite, focused on diagnosis and treatment. A deep understanding of the fluke’s molecular biology is underpinned by characterizing its genome. Today, we release an chromosome-length genome assembly for C. sinensis, produced using our existing short read assembly and new Hi-C data. The new assembly will provide a basis to conduct in-depth molecular studies of C. sinensis and broader comparative genomics and genetics of flatworms.

Read more here: Wang D, Young ND, Korhonen PK, Gasser RB. Clonorchis sinensis and Clonorchiasis: The Relevance of Exploring Genetic Variation. Adv Parasitol. 2018;100:155-208.

For the draft assembly used for this effort, please cite the following:

Wang D, Korhonen PK, Gasser RB, Young ND. Improved genomic resources and new bioinformatic workflow for the carcinogenic parasite Clonorchis sinensis: Biotechnological implications. Biotechnol Adv. 2018;36(4):894-904.

Acknowledgments:

We gratefully acknowledge the collaboration and samples provided Dr. Neil Young, The University of Melbourne. This work was supported in part by resources provided by DNA Zoo Australia, The University of Western Australia (UWA), with compute resource and support from the Pawsey Supercomputing Centre with funding from the Australian Government and the Government of Western Australia.