A Glycine max homolog of NON-RACE SPECIFIC DISEASE RESISTANCE 1 (NDR1) alters defense gene expression while functioning during a resistance response to different root pathogens in different genetic backgrounds

Abstract

A Glycine max homolog of the Arabidopsis thaliana NON-RACE SPECIFIC DISEASE RESISTANCE 1 (NDR1) coiled-coil nucleotide binding leucine rich repeat (CC-NB-LRR) defense signaling gene (Gm-NDR1-1) is expressed in root cells undergoing a defense response to the root pathogenic nematode, Heterodera glycines. Gm-NDR1-1 overexpression in the H. glycines-susceptible genotype G. max impairs parasitism. In contrast, Gm-NDR1-1 RNA interference (RNAi) in the H. glycines-resistant genotype G. max facilitates parasitism. The broad effectiveness of Gm-NDR1-1 in impairing parasitism has then been examined by engineering its heterologous expression in Gossypium hirsutum which is susceptible to the root pathogenic nematode Meloidogyne incognita. The heterologous expression of Gm-NDR1-1 in G. hirsutum effectively impairs M. incognita parasitism, reducing gall, egg mass, egg and juvenile numbers. In contrast to our prior experiments examining the effectiveness of the heterologous expression of a G. max homolog of the A. thaliana salicyclic acid signaling (SA) gene NONEXPRESSOR OF PR1 (Gm-NPR1-2), no cumulative negative effect on M. incognita parasitism has been observed in G. hirsutum expressing Gm-NDR1-1. The results indicate a common genetic basis exists for plant resistance to parasitic nematodes that involves Gm-NDR1. However, the Gm-NDR1-1 functions in ways that are measurably dissimilar to Gm-NPR1-2. Notably, Gm-NDR1-1 overexpression leads to increased relative transcript levels of its homologs of A. thaliana genes functioning in SA signaling, including NPR1-2, TGA2-1 and LESION SIMULATING DISEASE1 (LSD1-2) that is lost in Gm-NDR1-1 RNAi lines. Similar observations have been made regarding the expression of other defense genes.

Mitogen activated protein kinases function as a cohort during a plant defense response

“…Experiments presented here show that G. max MAPKs (MAPKs) identified to be expressed within parasitized root cells undergoing the process of defense to the root pathogenic nematode Heterodera glycines often presage their function in defense. Experiments show the relationship between PTI and ETI and the defense MAPKs to prior published work (Matsye et al 2011Pant et al 2014Pant et al , 2015Sharma et al 2016;McNeece et al 2017;Aljaafri et al 2017;. As presented in earlier experiments, PTI has been studied here by examining ENHANCED DISEASE SUSCEPTIBILITY1 (EDS1) and LESION SIMULATING DISEASE1 (LSD1) (Dietrich et al 1997;Aarts et al 1998;Falk et al 1999;Pant et al 2014Pant et al , 2015Matuszkiewicz et al 2018).…”

“…Employing transgenic approaches similar to those used to identify genes functioning in defense, an analysis is presented here examining each of the 32 members of the MAPK gene family of G. max in relation to its defense response during infection by a root pathogen (Bartsch et al 2006;Klink et al 2007Klink et al , 2010Klink et al , 2011Schmutz et al 2010;Grant et al 2010;Liu et al 2011;Goodstein et al 2012;Matsye et al 2012;Neupane et al 2013;Mohanta et al 2015;McNeece et al 2017). The G. max experimental system presents advantages over A. thaliana where a number of the defense genes have pleiotropic effects in single or combinatorially-mutated genetic backgrounds that result in highly compromised or lethal phenotypes (Lukowitz et al 1996;Heese et al 2001;Collins et al 2003;Assaad et al 2004;Zhang et al 2007;Lipka et al 2008;Han et al 2010;Humphry et al 2010;Huang et al 2010a;Heidrich et al 2011;Johansson et al 2014).…”

“…ETI has been studied by examining the relationship between treatment with bacterial elicitor harpin and MAPK gene expression . The experiments presented here then focus on G. max homologs of the ETI genes NON-RACE SPECIFIC DISEASE RESISTANCE 1/HARPIN INDUCED1 (NDR1/HIN1) and BOTRYTIS INDUCED KINASE1 (BIK1) (Wei et al 1992;Century et al 1995Century et al , 1997Gopalan et al 1996;Veronese et al 2006;McNeece et al 2017;Aljaafri et al 2017). Furthermore, transcriptional analyses show that the transgenic MAPK lines affect the expression of different suites of proven defense genes Pant et al 2014;Sharma et al 2016;McNeece et al 2017).…”

“…The experiments presented here then focus on G. max homologs of the ETI genes NON-RACE SPECIFIC DISEASE RESISTANCE 1/HARPIN INDUCED1 (NDR1/HIN1) and BOTRYTIS INDUCED KINASE1 (BIK1) (Wei et al 1992;Century et al 1995Century et al , 1997Gopalan et al 1996;Veronese et al 2006;McNeece et al 2017;Aljaafri et al 2017). Furthermore, transcriptional analyses show that the transgenic MAPK lines affect the expression of different suites of proven defense genes Pant et al 2014;Sharma et al 2016;McNeece et al 2017). These genes include those composing the PTI and ETI signal transduction cascades, the 20S membrane fusion particle, alpha hydroxynitrile biogenesis and cyanide metabolism, an ABC-G type transporter, carbon and hemicellulose metabolism and the expression of PATHOGENESIS RELATED1 (PR1) (Matsye et al 2011Pant et al 2014;Sharma et al 2016;McNeece et al 2017;.…”

Transcriptomic response in symptomless roots of clubroot infected kohlrabi (Brassica oleracea var. gongylodes) mirrors resistant plants

“…Those genes confer resistance to biotrophic bacterial pathogens in Arabidopsis 633 when recognizing effectors (Coppinger et al, 2004;Eitas et al, 2008). In roots of 634 beans, NDR1 also suppressed nematode parasitism by activating defence responses 635 (McNeece et al, 2017). Thus, we found indications that those proteins might also be 636 involved in a defence response towards P. brassicae.…”