TY - JOUR
T1 - A pathogenesis-related protein GmPR08-Bet VI promotes a molecular interaction between the GmSHMT08 and GmSNAP18 in resistance to Heterodera glycines
AU - Lakhssassi, Naoufal
AU - Piya, Sarbottam
AU - Bekal, Sadia
AU - Liu, Shiming
AU - Zhou, Zhou
AU - Bergounioux, Catherine
AU - Miao, Long
AU - Meksem, Jonas
AU - Lakhssassi, Aicha
AU - Jones, Karen
AU - Kassem, My Abdelmajid
AU - Benhamed, Moussa
AU - Bendahmane, Abdelhafid
AU - Lambert, Kris
AU - Boualem, Adnane
AU - Hewezi, Tarek
AU - Meksem, Khalid
N1 - Funding Information:
This research was supported in part from the United Soybean Board to (i) KM and KL, (ii) by a grant from USDA-NIFA # 2018-08232 to KM and NL, and (iii) was partially supported by funds from the Tennessee Soybean Promotion Board to the TH. We would like to thank Dr. Gunvant Patil for the haplotyping support and also Dr. Cyril Zipfel for providing the pGWB vectors for agroinfiltration experiments.
Funding Information:
This research was supported in part from the United Soybean Board to (i) KM and KL, (ii) by a grant from USDA‐NIFA # 2018‐08232 to KM and NL, and (iii) was partially supported by funds from the Tennessee Soybean Promotion Board to the TH. We would like to thank Dr. Gunvant Patil for the haplotyping support and also Dr. Cyril Zipfel for providing the pGWB vectors for agroinfiltration experiments.
Publisher Copyright:
© 2020 The Authors. Plant Biotechnology Journal published by Society for Experimental Biology and The Association of Applied Biologists and John Wiley & Sons Ltd.
PY - 2020/8/1
Y1 - 2020/8/1
N2 - Soybean cyst nematode (SCN, Heterodera glycines) is the most devastating pest affecting soybean production worldwide. SCN resistance requires both the GmSHMT08 and the GmSNAP18 in ‘Peking’-type resistance. Here, we describe the molecular interaction between GmSHMT08 and GmSNAP18, which is potentiated by a pathogenesis-related protein GmPR08-Bet VI. Like GmSNAP18 and GmSHMT08, GmPR08-Bet VI expression was induced in response to SCN and its overexpression decreased SCN cysts by 65% in infected transgenic soybean roots. Overexpression of GmPR08-Bet VI did not have an effect on SCN resistance when the two cytokinin-binding sites in GmPR08-Bet VI were mutated, indicating a new role of GmPR08-Bet VI in SCN resistance. GmPR08-Bet VI was mapped to a QTL for resistance to SCN using different mapping populations. GmSHMT08, GmSNAP18 and GmPR08-Bet VI localize to the cytosol and plasma membrane. GmSNAP18 expression and localization hyper-accumulated at the plasma membrane and was specific to the root cells surrounding the nematode in SCN-resistant soybeans. Genes encoding key components of the salicylic acid signalling pathway were induced under SCN infection. GmSNAP18 and GmPR08-Bet VI were also induced under salicylic acid and cytokinin exogenous treatments, while GmSHMT08 was induced only when the resistant GmSNAP18 was present, pointing to the presence of a molecular crosstalk between SCN-resistant genes and defence genes. Expression analysis of GmSHMT08 and GmSNAP18 identified the need of a minimum expression requirement to trigger the SCN resistance reaction. These results provide insight into a new response mechanism towards plant nematode resistance involving haplotype compatibility, gene dosage and hormone signalling.
AB - Soybean cyst nematode (SCN, Heterodera glycines) is the most devastating pest affecting soybean production worldwide. SCN resistance requires both the GmSHMT08 and the GmSNAP18 in ‘Peking’-type resistance. Here, we describe the molecular interaction between GmSHMT08 and GmSNAP18, which is potentiated by a pathogenesis-related protein GmPR08-Bet VI. Like GmSNAP18 and GmSHMT08, GmPR08-Bet VI expression was induced in response to SCN and its overexpression decreased SCN cysts by 65% in infected transgenic soybean roots. Overexpression of GmPR08-Bet VI did not have an effect on SCN resistance when the two cytokinin-binding sites in GmPR08-Bet VI were mutated, indicating a new role of GmPR08-Bet VI in SCN resistance. GmPR08-Bet VI was mapped to a QTL for resistance to SCN using different mapping populations. GmSHMT08, GmSNAP18 and GmPR08-Bet VI localize to the cytosol and plasma membrane. GmSNAP18 expression and localization hyper-accumulated at the plasma membrane and was specific to the root cells surrounding the nematode in SCN-resistant soybeans. Genes encoding key components of the salicylic acid signalling pathway were induced under SCN infection. GmSNAP18 and GmPR08-Bet VI were also induced under salicylic acid and cytokinin exogenous treatments, while GmSHMT08 was induced only when the resistant GmSNAP18 was present, pointing to the presence of a molecular crosstalk between SCN-resistant genes and defence genes. Expression analysis of GmSHMT08 and GmSNAP18 identified the need of a minimum expression requirement to trigger the SCN resistance reaction. These results provide insight into a new response mechanism towards plant nematode resistance involving haplotype compatibility, gene dosage and hormone signalling.
KW - SCN mechanism
KW - SCN-R model
KW - cytokinins
KW - gene dosage effect
KW - molecular crosstalk
KW - molecular trafficking
KW - protein–protein interaction
KW - salicylic acid
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UR - http://www.scopus.com/inward/citedby.url?scp=85079046344&partnerID=8YFLogxK
U2 - 10.1111/pbi.13343
DO - 10.1111/pbi.13343
M3 - Article
C2 - 31960590
AN - SCOPUS:85079046344
VL - 18
SP - 1810
EP - 1829
JO - Plant Biotechnology Journal
JF - Plant Biotechnology Journal
SN - 1467-7644
IS - 8
ER -