College of Education, Hangzhou Normal University, Hangzhou, 311121, Zhejiang, People's Republic of China.
Hangzhou Key Laboratory of Animal Adaptation and Evolution, College of Life and Environmental Sciences, Hangzhou Normal University, Hangzhou, 311121, Zhejiang, People's Republic of China.
Sci Rep. 2021 Mar 4;11(1):5246. doi: 10.1038/s41598-021-84760-2.
Glutamine:fructose-6-phosphate aminotransferase (GFAT) and phosphofructokinase (PFK) are enzymes related to chitin metabolism. RNA interference (RNAi) technology was used to explore the role of these two enzyme genes in chitin metabolism. In this study, we found that GFAT and PFK were highly expressed in the wing bud of Nilaparvata lugens and were increased significantly during molting. RNAi of GFAT and PFK both caused severe malformation rates and mortality rates in N. lugens. GFAT inhibition also downregulated GFAT, GNPNA, PGM1, PGM2, UAP, CHS1, CHS1a, CHS1b, Cht1-10, and ENGase. PFK inhibition significantly downregulated GFAT; upregulated GNPNA, PGM2, UAP, Cht2-4, Cht6-7 at 48 h and then downregulated them at 72 h; upregulated Cht5, Cht8, Cht10, and ENGase; downregulated Cht9 at 48 h and then upregulated it at 72 h; and upregulated CHS1, CHS1a, and CHS1b. In conclusion, GFAT and PFK regulated chitin degradation and remodeling by regulating the expression of genes related to the chitin metabolism and exert opposite effects on these genes. These results may be beneficial to develop new chitin synthesis inhibitors for pest control.
果糖-6-磷酸氨基转移酶(GFAT)和磷酸果糖激酶(PFK)是与几丁质代谢相关的酶。本研究采用 RNA 干扰(RNAi)技术,探讨了这两个酶基因在几丁质代谢中的作用。结果表明,GFAT 和 PFK 在褐飞虱翅芽中高表达,在蜕皮过程中显著上调。GFAT 和 PFK 的 RNAi 均导致褐飞虱严重畸形和死亡率。GFAT 抑制也下调了 GFAT、GNPNA、PGM1、PGM2、UAP、CHS1、CHS1a、CHS1b、Cht1-10 和 ENGase。PFK 抑制显著下调了 GFAT;48 h 时上调了 GNPNA、PGM2、UAP、Cht2-4、Cht6-7,72 h 时下调了它们;48 h 时上调了 Cht5、Cht8、Cht10 和 ENGase,72 h 时下调了 Cht9;上调了 CHS1、CHS1a 和 CHS1b。综上所述,GFAT 和 PFK 通过调节与几丁质代谢相关的基因表达,调控几丁质的降解和重塑,对这些基因发挥相反的作用。这些结果可能有助于开发新的几丁质合成抑制剂用于害虫防治。