Reference Report for AP20210630.1
| Title: | Syntaxin 31 functions in Glycine max resistance to the plant parasitic nematode Heterodera glycines. |
| Authors: | Pant, S.R., Matsye, P.D., McNeece, B.T., Sharma, K., Krishnavajhala, A., Lawrence. G.W., Klink, V.P. |
| Source: | Pant et al. 2014 Plant Mol. Biol., 85:107-121 |
| Abstract: | A Glycine max syntaxin 31 homolog (Gm-SYP38) was identified as being expressed in nematode-induced feeding structures known as syncytia undergoing an incompatible interaction with the plant parasitic nematode Heterodera glycines. The observed Gm-SYP38 expression was consistent with prior gene expression analyses that identified the alpha soluble NSF attachment protein (Gm--SNAP) resistance gene because homologs of these genes physically interact and function together in other genetic systems. Syntaxin 31 is a protein that resides on the cis face of the Golgi apparatus and binds -SNAP-like proteins, but has no known role in resistance. Experiments presented here show Gm--SNAP overexpression induces Gm-SYP38 transcription. Overexpression of Gm-SYP38 rescues G. max[Williams 82/PI 518671], genetically rhg1/, by suppressing H. glycines parasitism. In contrast, Gm-SYP38 RNAi in the rhg1+/+ genotype G. max[Peking/PI 548402] increases susceptibility. Gm--SNAP and Gm-SYP38 overexpression induce the transcriptional activity of the cytoplasmic receptor-like kinase BOTRYTIS INDUCED KINASE 1 (Gm-BIK1-6) which is a family of defense proteins known to anchor to membranes through a 5 MGXXXS/T(R) N-myristoylation sequence. Gm-BIK1-6 had been identified previously by RNA-seq experiments as expressed in syncytia undergoing an incompatible reaction. Gm-BIK1-6 overexpression rescues the resistant phenotype. In contrast, Gm-BIK1-6 RNAi increases parasitism. The analysis demonstrates a role for syntaxin 31-like genes in resistance that until now was not known. |
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