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N 6 -(2-Hydroxyethyl)-Adenosine Exhibits Insecticidal Activity against Plutella xylostella via Adenosine Receptors

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ABSTRACT

The diamondback moth, Plutella xylostella, is one of the most important pests of cruciferous crops. We have earlier shown that N6-(2-hydroxyethyl)-adenosine (HEA) exhibits insecticidal activity against P. xylostella. In the present study we investigated the possible mechanism of insecticidal action of HEA on P. xylostella. HEA is a derivative of adenosine, therefore, we speculated whether it acts via P. xylostella adenosine receptor (PxAdoR). We used RNAi approach to silence PxAdoR gene and used antagonist of denosine receptor (AdoR) to study the insecticidal effect of HEA. We cloned the whole sequence of PxAdoR gene. A BLAST search using NCBI protein database showed a 61% identity with the Drosophila adenosine receptor (DmAdoR) and a 32–35% identity with human AdoR. Though the amino acids sequence of PxAdoR was different compared to other adenosine receptors, most of the amino acids that are known to be important for adenosine receptor ligand binding and signaling were present. However, only 30% binding sites key residues was similar between PxAdoR and A1R. HEA, at a dose of 1 mg/mL, was found to be lethal to the second-instar larvae of P. xylostella, and a significant reduction of mortality and growth inhibition ratio were obtained when HEA was administered to the larvae along with PxAdoR-dsRNA or antagonist of AdoR (SCH58261) for 36, 48, or 60 h. Especially at 48 h, the rate of growth inhibition of the PxAdoR knockdown group was 3.5-fold less than that of the HEA group, and the corrected mortality of SCH58261 group was reduced almost 2-fold compared with the HEA group. Our findings show that HEA may exert its insecticidal activity against P. xylostella larvae via acting on PxAdoR.

No MeSH data available.


Impact of RNAi and Receptor Inhibitor on the insecticidal effect of HEA.Larvae were fed with dsRNA or receptor inhibitor (SCH58261) with or without HEA for a period of 24 h to 60 h. *P < 0.05; **P < 0.001 compared with the HEA group. (A) Effect of PxAdoR silencing and SCH58261 on the mortality induced by HEA. Corrected mortality (%) = (mortality of treatment−mortality of control)/(1−mortality of control)×100. (B) Effect of PxAdoR silencing on the rate of larvae growth. Rate of growth inhibition (%) = [(weight of control−weight of treatment)/ weight of control]×100.
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pone.0162859.g004: Impact of RNAi and Receptor Inhibitor on the insecticidal effect of HEA.Larvae were fed with dsRNA or receptor inhibitor (SCH58261) with or without HEA for a period of 24 h to 60 h. *P < 0.05; **P < 0.001 compared with the HEA group. (A) Effect of PxAdoR silencing and SCH58261 on the mortality induced by HEA. Corrected mortality (%) = (mortality of treatment−mortality of control)/(1−mortality of control)×100. (B) Effect of PxAdoR silencing on the rate of larvae growth. Rate of growth inhibition (%) = [(weight of control−weight of treatment)/ weight of control]×100.

Mentions: The mortality and rate of growth inhibition of the group fed with Pxds were the lowest compared to control group and the corrected mortality rates were found to be below 5% at 24, 36, 48, and 60 h time points. This data shows that Pxds feeding affected the insect body minimally. The corrected mortality of the Pxds–HEA group showed a significant reduction at all time points (24 h: from 12% to 6%; P < 0.05; 36 h: 14% to 4%; P < 0.001; 48 h: 29% to 6%; P < 0.001; 60 h: 29% to 11%; P < 0.001) compared with the HEA group at each time point. These results show that silencing PxAdoR gene can reduce the lethal effect of HEA on P. xylostella larvae. The corrected mortality of the SCH-HEA group at 24 h did not show a significant difference compared to the HEA group, however, a significant reduction in mortality was observed from 36 h to 60 h time points (P < 0.001). In particular, at 48 and 60 h, almost 2-fold reduction in mortality was observed (Fig 4A).


N 6 -(2-Hydroxyethyl)-Adenosine Exhibits Insecticidal Activity against Plutella xylostella via Adenosine Receptors
Impact of RNAi and Receptor Inhibitor on the insecticidal effect of HEA.Larvae were fed with dsRNA or receptor inhibitor (SCH58261) with or without HEA for a period of 24 h to 60 h. *P < 0.05; **P < 0.001 compared with the HEA group. (A) Effect of PxAdoR silencing and SCH58261 on the mortality induced by HEA. Corrected mortality (%) = (mortality of treatment−mortality of control)/(1−mortality of control)×100. (B) Effect of PxAdoR silencing on the rate of larvae growth. Rate of growth inhibition (%) = [(weight of control−weight of treatment)/ weight of control]×100.
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Related In: Results  -  Collection

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getmorefigures.php?uid=PMC5036850&req=5

pone.0162859.g004: Impact of RNAi and Receptor Inhibitor on the insecticidal effect of HEA.Larvae were fed with dsRNA or receptor inhibitor (SCH58261) with or without HEA for a period of 24 h to 60 h. *P < 0.05; **P < 0.001 compared with the HEA group. (A) Effect of PxAdoR silencing and SCH58261 on the mortality induced by HEA. Corrected mortality (%) = (mortality of treatment−mortality of control)/(1−mortality of control)×100. (B) Effect of PxAdoR silencing on the rate of larvae growth. Rate of growth inhibition (%) = [(weight of control−weight of treatment)/ weight of control]×100.
Mentions: The mortality and rate of growth inhibition of the group fed with Pxds were the lowest compared to control group and the corrected mortality rates were found to be below 5% at 24, 36, 48, and 60 h time points. This data shows that Pxds feeding affected the insect body minimally. The corrected mortality of the Pxds–HEA group showed a significant reduction at all time points (24 h: from 12% to 6%; P < 0.05; 36 h: 14% to 4%; P < 0.001; 48 h: 29% to 6%; P < 0.001; 60 h: 29% to 11%; P < 0.001) compared with the HEA group at each time point. These results show that silencing PxAdoR gene can reduce the lethal effect of HEA on P. xylostella larvae. The corrected mortality of the SCH-HEA group at 24 h did not show a significant difference compared to the HEA group, however, a significant reduction in mortality was observed from 36 h to 60 h time points (P < 0.001). In particular, at 48 and 60 h, almost 2-fold reduction in mortality was observed (Fig 4A).

View Article: PubMed Central - PubMed

ABSTRACT

The diamondback moth, Plutella xylostella, is one of the most important pests of cruciferous crops. We have earlier shown that N6-(2-hydroxyethyl)-adenosine (HEA) exhibits insecticidal activity against P. xylostella. In the present study we investigated the possible mechanism of insecticidal action of HEA on P. xylostella. HEA is a derivative of adenosine, therefore, we speculated whether it acts via P. xylostella adenosine receptor (PxAdoR). We used RNAi approach to silence PxAdoR gene and used antagonist of denosine receptor (AdoR) to study the insecticidal effect of HEA. We cloned the whole sequence of PxAdoR gene. A BLAST search using NCBI protein database showed a 61% identity with the Drosophila adenosine receptor (DmAdoR) and a 32&ndash;35% identity with human AdoR. Though the amino acids sequence of PxAdoR was different compared to other adenosine receptors, most of the amino acids that are known to be important for adenosine receptor ligand binding and signaling were present. However, only 30% binding sites key residues was similar between PxAdoR and A1R. HEA, at a dose of 1 mg/mL, was found to be lethal to the second-instar larvae of P. xylostella, and a significant reduction of mortality and growth inhibition ratio were obtained when HEA was administered to the larvae along with PxAdoR-dsRNA or antagonist of AdoR (SCH58261) for 36, 48, or 60 h. Especially at 48 h, the rate of growth inhibition of the PxAdoR knockdown group was 3.5-fold less than that of the HEA group, and the corrected mortality of SCH58261 group was reduced almost 2-fold compared with the HEA group. Our findings show that HEA may exert its insecticidal activity against P. xylostella larvae via acting on PxAdoR.

No MeSH data available.