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A  Leptinotarsa decemlineata  SLC6 NAT gene ( LdNAT1 ) was cloned.  LdNAT1  was highly expressed in the larval alimentary canal especially midgut.  LdNAT1  mRNA levels were high right after the molt and low just before the molt. JH and a JH analog pyriproxyfen activated  LdNAT1  expression. RNAi of an allatostatin gene  LdAS-C  increased JH and upregulated  LdNAT1  transcription. Conversely, silencing of a JH biosynthesis gene  LdJHAMT  decreased JH and reduced  LdNAT1  expression. Moreover, 20E and an ecdysteroid agonist halofenozide repressed  LdNAT1  expression, whereas a decrease in 20E by RNAi of an ecdysteroidogenesis gene  LdSHD  and disruption of 20E signaling by knockdown of  LdE75  and  LdFTZ-F1  activated  LdNAT1  expression. Thus,  LdNAT1  responded to both 20E and JH. Moreover, knockdown of  LdNAT1  reduced the contents of cysteine, histidine, isoleucine, leucine, methionine, phenylalanine and serine in the larval bodies and increased the contents of these amino acids in the larval feces. Furthermore, RNAi of  LdNAT1  inhibited insulin/target of rapamycin pathway, lowered 20E and JH titers, reduced 20E and JH signaling, retarded larval growth and impaired pupation. These data showed that  LdNAT1  was involved in the absorption of several neutral amino acids critical for larval growth and metamorphosis.

Knockdown of a nutrient amino acid transporter gene LdNAT1 reduces free neutral amino acid contents and impairs Leptinotarsa decemlineata pupation