February 23, 2016

Genome reveals insights into tick that spreads Lyme disease

At a Glance

  • Researchers deciphered the genome of the blacklegged tick, which causes several human diseases, including Lyme disease.
  • Understanding what makes ticks so effective at spreading diseases may lead to new ways to control them.
Blacklegged tick A blacklegged tick “questing” for a host on a blade of grass. CDC

Lyme disease, which is caused by the bacterium Borrelia burgdorferi, is transmitted to humans through the bite of an infected tick. It is the most common tickborne infectious disease in the United States. The blacklegged tick (Ixodes scapularis) is responsible for causing Lyme disease in North America, Europe, and Asia. Ixodes ticks spread other infectious agents as well, including those that cause human babesiosis, human granulocytic anaplasmosis, tick-borne relapsing fever, and Powassan encephalitis.

Deciphering the Ixodes genome would provide a powerful resource to help find ways of controlling these diseases. An international team headed by Dr. Catherine A. Hill of Purdue University worked for years to decipher the tick’s complicated genome. Ixodes ticks have 3 blood-feeding life stages and feed on a different vertebrate animal during each one. Because genes may switch on or off depending on the life stage of the tick, the ticks need to be cultured and collected at each stage for analysis. The study was supported by NIH’s National Institute of Allergy and Infectious Diseases (NIAID) and National Institute of General Medical Sciences (NIGMS). Results appeared on February 9, 2016, in Nature Communications.

The researchers determined that the Ixodes genome has about 2.1 billion DNA base pairs. A large portion of the genome—about 70% of the total—consists of expansive regions where sequences are repeated. This made assembling the full genome in the correct order very difficult. In the end, the team was able to determine the order and sequence of about two-thirds of the total genome—more than 20,000 protein-coding genes. About 20% of these, the researchers believe, may be unique to ticks.

The scientists identified genes and protein families that shed light on why Ixodes ticks succeed so well as parasites and hint at the reasons they excel at spreading pathogens. For example, compared with other blood-feeders, ticks have many more proteins devoted to consuming, concentrating, and detoxifying their iron-containing food. Although mosquitoes have several proteins dedicated to blood digestion, ticks have many more proteins involved in this process.

The tick’s genome reflects other peculiarities of their lifestyle. These include genes associated with the sensory systems that it uses when “questing” for a host during each of its separate blood-feeding stages.

In an effort to explain regional variations in Lyme disease prevalence across the United States, the team also examined genetic diversity among I. scapularis populations from several states. They detected subtle genetic differences that may help explain some of the variance in the ability to transmit disease.

“The genome gives us a code book to the inner workings of ticks,” Hill says. “With it, we can now begin to hack their system and write a counter-script against them.”

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Reference: Genomic insights into the Ixodes scapularis tick vector of Lyme disease. Gulia-Nuss M, Nuss AB, Meyer JM, Sonenshine DE, Roe RM, Waterhouse RM, Sattelle DB, de la Fuente J, Ribeiro JM, Megy K, Thimmapuram J, Miller JR, Walenz BP, Koren S, Hostetler JB, Thiagarajan M, Joardar VS, Hannick LI, Bidwell S, Hammond MP, Young S, Zeng Q, Abrudan JL, Almeida FC, Ayllón N, Bhide K, Bissinger BW, Bonzon-Kulichenko E, Buckingham SD, Caffrey DR, Caimano MJ, Croset V, Driscoll T, Gilbert D, Gillespie JJ, Giraldo-Calderón GI, Grabowski JM, Jiang D, Khalil SM, Kim D, Kocan KM, Koči J, Kuhn RJ, Kurtti TJ, Lees K, Lang EG, Kennedy RC, Kwon H, Perera R, Qi Y, Radolf JD, Sakamoto JM, Sánchez-Gracia A, Severo MS, Silverman N, Šimo L, Tojo M, Tornador C, Van Zee JP, Vázquez J, Vieira FG, Villar M, Wespiser AR, Yang Y, Zhu J, Arensburger P, Pietrantonio PV, Barker SC, Shao R, Zdobnov EM, Hauser F, Grimmelikhuijzen CJ, Park Y, Rozas J, Benton R, Pedra JH, Nelson DR, Unger MF, Tubio JM, Tu Z, Robertson HM, Shumway M, Sutton G, Wortman JR, Lawson D, Wikel SK, Nene VM, Fraser CM, Collins FH, Birren B, Nelson KE, Caler E, Hill CA. Nat Commun. 2016 Feb 9;7:10507. doi: 10.1038/ncomms10507. PMID: 26856261.

Funding: NIH’s National Institute of Allergy and Infectious Diseases (NIAID) and National Institute of General Medical Sciences (NIGMS).