Akt is an essential player in regulating cell/organ growth at the adult stage in the hard tick Haemaphysalis longicornis.

Ticks grow rapidly during blood feeding, and their body weight may ultimately increase 100-fold more than that before feeding. The molecular mechanisms controlling growth during blood feeding in ticks remain largely unknown. The conserved insulin/PI3K/Akt signaling pathway regulates growth and metabolism in eukaryotes. Here, we show evidence for the involvement of Akt in growth during blood feeding in the parthenogenetic strain of the hard tick Haemaphysalis longicornis. We identified a homolog of the Ser/Thr kinase Akt (HlAkt) from the EST database of the H. longicornis embryo. HlAkt cDNA had a 1,590 bp ORF that encodes 529 amino acids with a predicted molecular weight of 60 kDa. HlAkt possesses a PH domain, a Ser/Thr kinase domain, a hydrophobic motif, and dual phosphorylation residues (Thr 338 and Ser 503) that are essential for kinase activation. Knockdown of HlAkt by RNA interference caused inhibition of blood feeding in female ticks. Histological observation demonstrated that HlAkt knockdown led to the arrest of growth in internal organs. HlAkt knockdown also affected the expressions of blood meal-induced genes that are essential for blood digestion, development, and reproduction in the female tick. These results strongly indicate that HlAkt is essential to complete the blood feeding process accompanied by the growth of internal organs in adult ticks. This is the first report of identification and characterization of Akt in Chelicerata, including ticks.