کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
1981925 1539475 2016 17 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Physiological roles of trehalose in Leptinotarsa larvae revealed by RNA interference of trehalose-6-phosphate synthase and trehalase genes
ترجمه فارسی عنوان
نقش فیزیولوژیک ترهالوز در لارو Leptinotarsa نشان داد توسط تداخل RNA ژن سنتاز و trehalase ترهالوز-6-فسفات
موضوعات مرتبط
علوم زیستی و بیوفناوری علوم کشاورزی و بیولوژیک دانش حشره شناسی
چکیده انگلیسی


• Trehalose-6-phosphate synthase (LdTPS) and trehalase genes (LdTRE1a or LdTRE2) were cloned.
• Knockdown of LdTPS decreased but silencing of LdTRE1a or LdTRE2 increased trehalose contents in Leptinotarsa decemlineata larvae.
• The LdTPS RNAi survivors consumed more but the LdTRE1a RNAi hypomorphs fed less foliage.
• The LdTPS RNAi larvae were fat in contrast to the LdTRE1a RNAi hypomorphs.
• LdTPS and LdTRE1a RNAi reduced chitin contents.
• LdTPS, LdTRE1a and LdTRE2 RNAi caused lethality.

Trehalose is proposed to serve multiple physiological roles in insects. However, its importance remains largely unconfirmed. In the present paper, we knocked down either a trehalose biosynthesis gene (trehalose-6-phosphate synthase, LdTPS) or each of three degradation genes (soluble trehalases LdTRE1a, LdTRE1b or membrane-bound LdTRE2) in Leptinotarsa decemlineata by RNA interference (RNAi). Knockdown of LdTPS decreased trehalose content and caused larval and pupal lethality. The LdTPS RNAi survivors consumed a greater amount of foliage, obtained a heavier body mass, accumulated more glycogen, lipid and proline, and had a smaller amount of chitin compared with the controls. Ingestion of trehalose but not glucose rescued the food consumption increase and larval mass rise, increased survivorship, and recovered glycogen, lipid and chitin to the normal levels. In contrast, silencing of LdTRE1a increased trehalose content and resulted in larval and pupal lethality. The surviving LdTRE1a RNAi hypomorphs fed a smaller quantity of food, had a lighter body weight, depleted lipid and several glucogenic amino acids, and contained a smaller amount of chitin. Neither trehalose nor glucose ingestion rescued these LdTRE1a RNAi defects. Silencing of LdTRE1b caused little effects. Knockdown of LdTRE2 caused larval death, increased trehalose contents in several tissues and diminished glycogen in the brain-corpora cardiaca-corpora allata complex (BCC). Feeding glucose but not trehalose partially rescued the high mortality rate and recovered glycogen content in the BCC. It seems that trehalose is involved in feeding regulation, sugar absorption, brain energy supply and chitin biosynthesis in L. decemlineata larvae.

Figure optionsDownload high-quality image (221 K)Download as PowerPoint slide

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Insect Biochemistry and Molecular Biology - Volume 77, October 2016, Pages 52–68
نویسندگان
, , , , , , ,