The peritrophic membrane (or peritrophic matrix) (PM) in insects is formed by binding of PM proteins with multiple chitin binding domains (CBDs) to chitin fibrils. Multi-CBD chitin binding proteins (CBPs) and the insect intestinal mucin (IIM) are major PM structural proteins. To understand the biochemical and physiological role of IIM in structural formation and physiological function of the PM, Trichoplusia ni mutant strains lacking IIM were generated by CRISPR/Cas9 mutagenesis. The mutant T. ni larvae were confirmed to lack IIM, but PM formation was observed as in wild type larvae and lacking IIM in the PM did not result in changes of protease activities in the larval midgut. Larval growth and development of the mutant strains were similar to the wild type strain on artificial diet and cabbage leaves, but had a decreased survival in the 5th instar. The larvae of the mutant strains with the PM formed without IIM did not have a change of susceptibility to the infection of the baculovirus AcMNPV and the Bacillus thuringiensis (Bt) formulation Dipel, to the toxicity of the Bt toxins Cry1Ac and Cry2Ab and the chemical insecticide sodium aluminofluoride. Treatment of the mutant T. ni larvae with Calcofluor reduced the larval susceptibility to the toxicity of Bt Cry1Ac, as similarly observed in the wild type larvae. Overall, in the mutant T. ni larvae, the PM was formed without IIM and the lacking of IIM in the PM did not drastically impact the performance of larvae on diet or cabbage leaves under the laboratory conditions.

昆虫中的营养膜（或营养膜）（PM）是通过将具有多个几丁质结合域（CBD）的PM蛋白与几丁质原纤维结合而形成的。多CBD几丁质结合蛋白（CBPs）和昆虫肠道粘蛋白（IIM）是主要的PM结构蛋白。为了了解IIM在PM的结构形成和生理功能中的生化和生理作用，通过CRISPR / Cas9诱变产生了缺乏IIM的Trichoplusia ni突变株。突变体T. ni幼虫被证实缺乏IIM，但是观察到PM形成如野生型幼虫，并且PM中缺乏IIM并没有导致幼虫中肠蛋白酶活性的改变。在人工饮食和甘蓝叶上，突变菌株的幼虫生长和发育与野生型菌株相似，但是在第5龄幼虫的存活期降低。没有IIM形成PM的突变菌株的幼虫对杆状病毒AcMNPV和苏云金芽孢杆菌（Bt）制剂Dipel的感染，对Bt毒素Cry1Ac和Cry2Ab以及化学杀虫剂的毒性的敏感性没有变化氟化铝钠。突变体T. ni的治疗与在野生型幼虫中观察到的相似，含钙氟龙的幼虫降低了幼虫对Bt Cry1Ac毒性的敏感性。总的来说，在突变体T. ni幼虫中，PM的形成没有IIM，并且在实验室条件下，PM中IIM的缺乏不会严重影响幼虫对饮食或卷心菜叶片的性能。