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The endomembrane system, functioning in secretion, performs many roles relating to eukaryotic cell physiological processes and the Golgi apparatus is the central organelle in this system. An essential associated Golgi component is the conserved oligomeric Golgi (COG) complex, maintaining correct Golgi structure and function during retrograde trafficking. In animals, naturally occurring cog mutants provide a window into understanding it's function(s). Eliminating even one COG component impairs its function. In animals, COG mutations lead to severe cell biological and developmental defects and death while far less is understood in plants which is changing. The plant genetic model Arabidopsis thaliana COG complex functions in growth, cell expansion and other processes, involving direct interactions with other secretion system components including the exocyst, soluble N-Ethylmaleimide-Sensitive Factor Attachment Protein Receptor (SNARE), and the microtubule cytoskeleton. Recent experiments have identified a defense role for the COG complex in plants, the focus of this review. [ABSTRACT FROM AUTHOR]

Abstract: The plant parasitic nematode, Heterodera glycines is the major pathogen of Glycine max (soybean). H. glycines accomplish parasitism by creating a nurse cell known as the syncytium from which it feeds. The syncytium undergoes two developmental phases. The first is a parasitism phase where feeding sites are selected, initiating the development of the syncytium. During this earlier phase (1–4 days post infection), syncytia undergoing resistant and susceptible reactions appear the same. The second phase is when the resistance response becomes evident (between 4 and 6dpi) and is completed by 9dpi. Analysis of the resistant reaction of G. max genotype PI 88788 (G. max [PI 88788]) to H. glycines population NL1-RHg/HG-type 7 (H. glycines [NL1-RHg/HG-type 7]) is accomplished by laser microdissection of syncytia at 3, 6 and 9dpi. Comparative analyses are made to pericycle and their neighboring cells isolated from mock-inoculated roots. These analyses reveal induced levels of the jasmonic acid biosynthesis and 13-lipoxygenase pathways. Direct comparative analyses were also made of syncytia at 6 days post infection to those at 3dpi (base line). The comparative analyses were done to identify localized gene expression that characterizes the resistance phase of the resistant reaction. The most highly induced pathways include components of jasmonic acid biosynthesis, 13-lipoxygenase pathway, S-adenosyl methionine pathway, phenylpropanoid biosynthesis, suberin biosynthesis, adenosylmethionine biosynthesis, ethylene biosynthesis from methionine, flavonoid biosynthesis and the methionine salvage pathway. In comparative analyses of 9dpi to 6dpi (base line), these pathways, along with coumarin biosynthesis, cellulose biosynthesis and homogalacturonan degradation are induced. The experiments presented here strongly implicate the jasmonic acid defense pathway as a factor involved in the localized resistant reaction of G. max [PI 88788] to H. glycines [NL1-RHg/HG-type 7]. [Copyright &y& Elsevier]

Expression of the central circadian oscillator components CIRCADIAN CLOCK ASSOCIATED 1 (CCA1), TIMING OF CAB1 (TOC1), GIGANTEA (GI), and CONSTANS (CO) occurs in Glycine max root cells (syncytia) parasitized by the nematode Heterodera glycines while undergoing resistance, indicating a defense role. GmCCA1-1 relative transcript abundance (RTA) in roots experiencing overexpression (OE) or RNA interference (RNAi) is characterized by rhythmic oscillations, compared to a ribosomal protein gene (GmRPS21) control. A GmCCA1-1 RTA change, advancing by 12 h, exists in H. glycines -infected as compared to uninfected controls in wild-type, H. glycines -resistant, G. max [Peking/PI 548402]. The G. max [Peking/PI 548402] transgenic controls exhibit the RTA change by 4 h post infection (hpi), not consistently occurring in the H. glycines -susceptible G. max [Williams 82/PI 518671] until 56 hpi. GmCCA1-1 expression is observed to be reduced in H. glycines -infected GmCCA1-1 -OE roots as compared to non-infected transgenic roots with no significant change observed among RNAi roots. The GmCCA1-1 expression in transgenic GmCCA1-1 -OE roots remains higher than control and RNAi roots. Decreased GmCCA1-1 mRNA among infected roots shows the altered expression is targeted by H. glycines. Gene expression of proven defense genes including 9 different mitogen activated protein kinases (GmMAPK s), NON-RACE SPECIFIC DISEASE RESISTANCE 1 (GmNDR1-1), RPM1-INTERACTING PROTEIN 4 (GmRIN4-4), and the secreted xyloglucan endotransglycosylase/hydrolase 43 (GmXTH43) in GmCCA1- 1-OE and GmCCA1-1 -RNAi roots, compared to controls, reveal a significant role of GmCCA1-1 expression in roots undergoing defense to H. glycines parasitism. The observation that GmCCA1-1 regulates GmXTH43 expression links the central circadian oscillator to the functionality of the secretion system. • Central circadian oscillator genes are expressed in nematode-parasitized root cells undergoing defense. • The overexpression of the central circadian oscillator genes suppresses parasitism. • The central circadian oscillator gene CCA1-1 regulates the expression of proven defense genes. [ABSTRACT FROM AUTHOR]

Pathogen-secreted polygalacturonases (PGs) alter plant cell wall structure by cleaving the α-(1 → 4) linkages between D-galacturonic acid residues in homogalacturonan (HG), macerating the cell wall, facilitating infection. Plant PG inhibiting proteins (PGIPs) disengage pathogen PGs, impairing infection. The soybean cyst nematode, Heterodera glycines , obligate root parasite produces secretions, generating a multinucleate nurse cell called a syncytium, a byproduct of the merged cytoplasm of 200–250 root cells, occurring through cell wall maceration. The common cytoplasmic pool, surrounded by an intact plasma membrane, provides a source from which H. glycines derives nourishment but without killing the parasitized cell during a susceptible reaction. The syncytium is also the site of a naturally-occurring defense response that happens in specific G. max genotypes. Transcriptomic analyses of RNA isolated from the syncytium undergoing the process of defense have identified that one of the 11 G. max PGIP s, GmPGIP11 , is expressed during defense. Functional transgenic analyses show roots undergoing GmPGIP11 overexpression (OE) experience an increase in its relative transcript abundance (RTA) as compared to the ribosomal protein 21 (GmRPS21) control, leading to a decrease in H. glycines parasitism as compared to the overexpression control. The GmPGIP11 undergoing RNAi experiences a decrease in its RTA as compared to the GmRPS21 control with transgenic roots experiencing an increase in H. glycines parasitism as compared to the RNAi control. Pathogen associated molecular pattern (PAMP) triggered immunity (PTI) and effector triggered immunity (ETI) components are shown to influence GmPGIP11 expression while numerous agricultural crops are shown to have homologs. [Display omitted] • The complete Glycine max (soybean) polygalacturonase inhibiting protein (PGIP) protein family is identified. • The expression of soybean PGIP gene family members are investigated. • A PGIP that is expressed in a pathogen infection site during defense functions in defense. [ABSTRACT FROM AUTHOR]

Soybean ( Glycine max ) infection by the charcoal rot (CR) ascomycete Macrophomina phaseolina is enhanced by the soybean cyst nematode (SCN) Heterodera glycines . We hypothesized that G. max genetic lines impairing infection by M. phaseolina would also limit H. glycines parasitism, leading to resistance. As a part of this M. phaseolina resistance process, the genetic line would express defense genes already proven to impair nematode parasitism. Using G. max [DT97-4290/PI 642055] , exhibiting partial resistance to M. phaseolina , experiments show the genetic line also impairs H. glycines parasitism. Furthermore, comparative studies show G. max [DT97-4290/PI 642055] exhibits induced expression of the effector triggered immunity (ETI) gene NON-RACE SPECIFIC DISEASE RESISTANCE 1/HARPIN INDUCED1 (NDR1/HIN1) that functions in defense to H. glycines as compared to the H. glycines and M. phaseolina susceptible line G. max [Williams 82/PI 518671] . Other defense genes that are induced in G. max [DT97-4290/PI 642055] include the pathogen associated molecular pattern (PAMP) triggered immunity (PTI) genes ENHANCED DISEASE SUSCEPTIBILITY1 (EDS1), NONEXPRESSOR OF PR1 (NPR1) and TGA2. These observations link G. max defense processes that impede H. glycines parasitism to also potentially function toward impairing M. phaseolina pathogenicity. Testing this hypothesis, G. max [Williams 82/PI 518671] genetically engineered to experimentally induce GmNDR1-1, EDS1-2, NPR1-2 and TGA2-1 expression leads to impaired M. phaseolina pathogenicity. In contrast, G. max [DT97-4290/PI 642055] engineered to experimentally suppress the expression of GmNDR1-1, EDS1-2, NPR1-2 and TGA2-1 by RNA interference (RNAi) enhances M. phaseolina pathogenicity. The results show components of PTI and ETI impair both nematode and M. phaseolina pathogenicity. [ABSTRACT FROM AUTHOR]