The heterologous expression of conserved Glycine max (soybean) mitogen activated protein kinase 3 (MAPK3) paralogs suppresses Meloidogyne incognita parasitism in Gossypium hirsutum (upland cotton)

Abstract

Two conserved Glycine max (soybean) mitogen activated protein kinase 3 (MAPK3) paralogs function in defense to the parasitic soybean cyst nematode Heterodera glycines. Gene Ontology analyses of RNA seq data obtained from MAPK3-1-overexpressing (OE) and MAPK3-2-OE roots compared to their control, as well as MAPK3-1-RNA interference (RNAi) and MAPK3-2-RNAi compared to their control, hierarchically orders the induced and suppressed genes, strengthening the hypothesis that their heterologous expression in Gossypium hirsutum (upland cotton) would impair parasitism by the root knot nematode (RKN) Meloidogyne incognita. MAPK3-1 expression (E) in G. hirsutum suppresses the production of M. incognita root galls, egg masses, and second stage juveniles (J2s) by 80.32%, 82.37%, and 88.21%, respectfully. Unexpectedly, egg number increases by 28.99% but J2s are inviable. MAPK3-2-E effects are identical, statistically. MAPK3-1-E and MAPK3-2-E decreases root mass 1.49-fold and 1.55-fold, respectively, as compared to the pRAP15-ccdB-E control. The reproductive factor (RF) of M. incognita for G. hirsutum roots expressing MAPK3-1-E or MAPK3-2-E decreases 60.39% and 50.46%, respectively, compared to controls. The results are consistent with upstream pathogen activated molecular pattern (PAMP) triggered immunity (PTI) and effector triggered immunity (ETI) functioning in defense to H. glycines. The experiments showcase the feasibility of employing MAPK3, through heterologous expression, to combat M. incognita parasitism, possibly overcoming impediments otherwise making G. hirsutum’s defense platform deficient. MAPK homologs are identified in other important crop species for future functional analyses.

Glycine maxpolygalacturonase inhibiting protein 11 (GmPGIP11) functions in the root to suppressHeterodera glycinesparasitism

“…It appears as though GmPGIP11 did not increase its RTA through induced GmMAPK3-1 or GmMAPK3-2 expression. This observation is surprising since the overexpression of GmBAK1-1- (Klink et al 2011).…”

“…GmMAPK3-1 and GmMAPK3-2 induce the expression of a common set of GmPGIPs including Glyma.05G123700, Glyma.05G123900, and Glyma.08G078900 (Klink et al 2022). The transcriptomic experiments also show that…”

“…GmMAPK3-1 and GmMAPK3-2 induce the expression of an AtPEPR1 PRR co-receptor homolog Glyma.10G195700 (GmBAK1-1), which functions in the defense response to H. glycines (Liu et al 2013;Jing et al 2020;Klink et al , 2022. This discovery is noteworthy because in A. thaliana PEPR1 recognizes short peptides which then activates BAK1 and BIK1 to promote defense responses through MAPK signaling (Liu et al 2013).…”

“…Gma.6599.1.S1_at (GmPG049) (Klink et al 2011). Klink et al (2011) then performed cross-comparative analyses between the previously studied 0, 3, 6 and 9 dpi time points of G. max [Peking/PI 548402] and G. max [PI 88788] .…”

“…Gma.6599.1.S1_at (GmPG049) (Klink et al 2011). Klink et al (2011) then performed cross-comparative analyses between the previously studied 0, 3, 6 and 9 dpi time points of G. max [Peking/PI 548402] and G. max [PI 88788] . In the first analysis of the 0 dpi pericycle control, no PGIPs were found to be expressed at a higher level in G. max [Peking/PI 548402] as The RTA of the candidate defense genes, presented as a FC, in the transgenic roots was compared GmRPS21 .…”