Spätzle1 is a constituent of the extracellular signaling pathway that promotes nodule formation, a cell‐mediated immune response, in caterpillar hemolymph. Issue 1 (7th October 2022)

• Record Type: Journal Article
• Authors: Tang, Shuyi; Tezuka, Moeko; Otsuka, Hinata; Sato, Ryoichi
• Is Part Of: Archives of insect biochemistry and physiology. Volume 112:Issue 1(2023)
• Page Start: n/a
• Page End: n/a
• Publication Date: 2022-10-07
• Subjects: Bombyx mori -- extracellular signaling pathway -- nodule formation -- Spätzle1; Insects -- Physiology -- Periodicals; Insect biochemistry -- Periodicals; 595.701572
• DOI: 10.1002/arch.21975
• Languages: English
• ISSNs: 0739-4462

Abstract

Abstract: The existence of an extracellular signaling pathway that mediates nodule formation, a cell‐mediated immune response, has been reported in Bombyx mori larvae. In this pathway, C‐type lectins and the hemolymph serine proteinase Bm HP‐8 function in pathogen associated molecular pattern (PAMPs) recognition and signaling transduction. However, which molecule elicits the cellular response at the end of the pathway is unknown. In this study, the Toll ligand Bombyx mori Spätzel1 was shown to be involved in the pathway by applying anit‐Spätzel1 antiserum in an in vitro nodule‐like aggregate formation assay and an in vivo nodule formation assay. Abstract : Anti‐Spätzle1 antiserum inhibited in vitro nodule‐like aggregates formation and in vivo nodule formation. Activated BmSPZ1 was detected from the hemocytes collected after injection of Saccharomyces cerevisiae cells, but not from the hemolymph. These suggest that Spätzle1 is involved in the extracellular nodule formation‐inducing signal pathway and that Spätzle1 might have soon bind to a putative receptor Toll on the hemocytes that were surrounding S. cerevisiae cells. Research Highlights: Anti‐Spätzle1 antiserum inhibited nodule formation. Activated BmSPZ1 was detected from only hemocytes collected after injection of Saccharomyces cerevisiae cells. Spätzle1 was suggested to be involved in nodule formation‐inducing signal pathway.