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Transcript dynamics at early stages of molecular interactions of MYMIV with resistant and susceptible genotypes of the leguminous host, Vigna mungo.

Kundu A, Patel A, Paul S, Pal A - PLoS ONE (2015)

Bottom Line: A significant fraction of modulated transcripts are of unknown function indicating participation of novel candidate genes in restricting this viral pathogen.T9 is perhaps due to the poor execution of these transcript modulation exhibiting remarkable repression of photosynthesis related genes resulting in chlorosis of leaves followed by penalty in crop yield.In addition to inflate the existing knowledge base, the genomic resources identified in this orphan crop would be useful for integrating MYMIV-tolerance trait in susceptible cultivars of V. mungo.

View Article: PubMed Central - PubMed

Affiliation: Division of Plant Biology, Bose Institute, Kolkata 700054, West Bengal, India.

ABSTRACT
Initial phases of the MYMIV-Vigna mungo interaction is crucial in determining the infection phenotype upon challenging with the virus. During incompatible interaction, the plant deploys multiple stratagems that include extensive transcriptional alterations defying the virulence factors of the pathogen. Such molecular events are not frequently addressed by genomic tools. In order to obtain a critical insight to unravel how V. mungo respond to Mungbean yellow mosaic India virus (MYMIV), we have employed the PCR based suppression subtractive hybridization technique to identify genes that exhibit altered expressions. Dynamics of 345 candidate genes are illustrated that differentially expressed either in compatible or incompatible reactions and their possible biological and cellular functions are predicted. The MYMIV-induced physiological aspects of the resistant host include reactive oxygen species generation, induction of Ca2+ mediated signaling, enhanced expression of transcripts involved in phenylpropanoid and ubiquitin-proteasomal pathways; all these together confer resistance against the invader. Elicitation of genes implicated in salicylic acid (SA) pathway suggests that immune response is under the regulation of SA signaling. A significant fraction of modulated transcripts are of unknown function indicating participation of novel candidate genes in restricting this viral pathogen. Susceptibility on the other hand, as exhibited by V. mungo Cv. T9 is perhaps due to the poor execution of these transcript modulation exhibiting remarkable repression of photosynthesis related genes resulting in chlorosis of leaves followed by penalty in crop yield. Thus, the present findings revealed an insight on the molecular warfare during host-virus interaction suggesting plausible signaling mechanisms and key biochemical pathways overriding MYMIV invasion in resistant genotype of V. mungo. In addition to inflate the existing knowledge base, the genomic resources identified in this orphan crop would be useful for integrating MYMIV-tolerance trait in susceptible cultivars of V. mungo.

No MeSH data available.


Related in: MedlinePlus

Hypothetical diagram illustrating the molecular mechanism of V. mungo resistance to MYMIV.The pathway is based on the integrated information collected from the differentially expressed ESTs. NBS LRR: Nucleotide binding site Leucine rich repeat, HSP90: Heat shock protein 90, SGT1: Suppressor of G2 allele of skp1, RAR1: required for Mla12 resistance; MAPK: ROS: Reactive oxygen species; MAP kinases, CAmml: Calmodulin, CaBP: Calcium binding protein, CDPKs: Calcium dependent protein kinases, PAL: Phenylalanine ammonia lyase, SA: Salicylic acid; 26S: UPS: Ubiquitin proteasome system, TFs: Transcription factors, ZF: Zinc finger, bHLH: Basic helix loop helix, WRKY. Bars represent mean ± standard deviation; bars followed by different letters indicate significant differences at p ≤ 0.05 according to DMRT.
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pone.0124687.g006: Hypothetical diagram illustrating the molecular mechanism of V. mungo resistance to MYMIV.The pathway is based on the integrated information collected from the differentially expressed ESTs. NBS LRR: Nucleotide binding site Leucine rich repeat, HSP90: Heat shock protein 90, SGT1: Suppressor of G2 allele of skp1, RAR1: required for Mla12 resistance; MAPK: ROS: Reactive oxygen species; MAP kinases, CAmml: Calmodulin, CaBP: Calcium binding protein, CDPKs: Calcium dependent protein kinases, PAL: Phenylalanine ammonia lyase, SA: Salicylic acid; 26S: UPS: Ubiquitin proteasome system, TFs: Transcription factors, ZF: Zinc finger, bHLH: Basic helix loop helix, WRKY. Bars represent mean ± standard deviation; bars followed by different letters indicate significant differences at p ≤ 0.05 according to DMRT.

Mentions: Typically, the resistance machinery is recruited upon perception of the invader that activates immune signaling and provides necessary arsenal to arrest pathogen proliferation. In the present study, a comparative transcriptional profiling was conducted to get an insight on the functional and regulatory networks of the early MYMIV stress-responsive genes, based on which a hypothetical model illustrating resistance mechanism operative in V. mungo against MYMIV has been proposed (Fig 6). Although a broad transcriptional inflection was observed, yet the modulated transcripts do not exhibit any explicit machinery associated with susceptibility. Here compatibility seems to be a consequence of the weak implementation of pathways that are strongly enforced by the resistant host against the intruder. This may be due to the absence of requisite signaling in the susceptible genotype in absence of the candidate resistance gene, CYR1, as shown by Maiti et al [13].


Transcript dynamics at early stages of molecular interactions of MYMIV with resistant and susceptible genotypes of the leguminous host, Vigna mungo.

Kundu A, Patel A, Paul S, Pal A - PLoS ONE (2015)

Hypothetical diagram illustrating the molecular mechanism of V. mungo resistance to MYMIV.The pathway is based on the integrated information collected from the differentially expressed ESTs. NBS LRR: Nucleotide binding site Leucine rich repeat, HSP90: Heat shock protein 90, SGT1: Suppressor of G2 allele of skp1, RAR1: required for Mla12 resistance; MAPK: ROS: Reactive oxygen species; MAP kinases, CAmml: Calmodulin, CaBP: Calcium binding protein, CDPKs: Calcium dependent protein kinases, PAL: Phenylalanine ammonia lyase, SA: Salicylic acid; 26S: UPS: Ubiquitin proteasome system, TFs: Transcription factors, ZF: Zinc finger, bHLH: Basic helix loop helix, WRKY. Bars represent mean ± standard deviation; bars followed by different letters indicate significant differences at p ≤ 0.05 according to DMRT.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4401676&req=5

pone.0124687.g006: Hypothetical diagram illustrating the molecular mechanism of V. mungo resistance to MYMIV.The pathway is based on the integrated information collected from the differentially expressed ESTs. NBS LRR: Nucleotide binding site Leucine rich repeat, HSP90: Heat shock protein 90, SGT1: Suppressor of G2 allele of skp1, RAR1: required for Mla12 resistance; MAPK: ROS: Reactive oxygen species; MAP kinases, CAmml: Calmodulin, CaBP: Calcium binding protein, CDPKs: Calcium dependent protein kinases, PAL: Phenylalanine ammonia lyase, SA: Salicylic acid; 26S: UPS: Ubiquitin proteasome system, TFs: Transcription factors, ZF: Zinc finger, bHLH: Basic helix loop helix, WRKY. Bars represent mean ± standard deviation; bars followed by different letters indicate significant differences at p ≤ 0.05 according to DMRT.
Mentions: Typically, the resistance machinery is recruited upon perception of the invader that activates immune signaling and provides necessary arsenal to arrest pathogen proliferation. In the present study, a comparative transcriptional profiling was conducted to get an insight on the functional and regulatory networks of the early MYMIV stress-responsive genes, based on which a hypothetical model illustrating resistance mechanism operative in V. mungo against MYMIV has been proposed (Fig 6). Although a broad transcriptional inflection was observed, yet the modulated transcripts do not exhibit any explicit machinery associated with susceptibility. Here compatibility seems to be a consequence of the weak implementation of pathways that are strongly enforced by the resistant host against the intruder. This may be due to the absence of requisite signaling in the susceptible genotype in absence of the candidate resistance gene, CYR1, as shown by Maiti et al [13].

Bottom Line: A significant fraction of modulated transcripts are of unknown function indicating participation of novel candidate genes in restricting this viral pathogen.T9 is perhaps due to the poor execution of these transcript modulation exhibiting remarkable repression of photosynthesis related genes resulting in chlorosis of leaves followed by penalty in crop yield.In addition to inflate the existing knowledge base, the genomic resources identified in this orphan crop would be useful for integrating MYMIV-tolerance trait in susceptible cultivars of V. mungo.

View Article: PubMed Central - PubMed

Affiliation: Division of Plant Biology, Bose Institute, Kolkata 700054, West Bengal, India.

ABSTRACT
Initial phases of the MYMIV-Vigna mungo interaction is crucial in determining the infection phenotype upon challenging with the virus. During incompatible interaction, the plant deploys multiple stratagems that include extensive transcriptional alterations defying the virulence factors of the pathogen. Such molecular events are not frequently addressed by genomic tools. In order to obtain a critical insight to unravel how V. mungo respond to Mungbean yellow mosaic India virus (MYMIV), we have employed the PCR based suppression subtractive hybridization technique to identify genes that exhibit altered expressions. Dynamics of 345 candidate genes are illustrated that differentially expressed either in compatible or incompatible reactions and their possible biological and cellular functions are predicted. The MYMIV-induced physiological aspects of the resistant host include reactive oxygen species generation, induction of Ca2+ mediated signaling, enhanced expression of transcripts involved in phenylpropanoid and ubiquitin-proteasomal pathways; all these together confer resistance against the invader. Elicitation of genes implicated in salicylic acid (SA) pathway suggests that immune response is under the regulation of SA signaling. A significant fraction of modulated transcripts are of unknown function indicating participation of novel candidate genes in restricting this viral pathogen. Susceptibility on the other hand, as exhibited by V. mungo Cv. T9 is perhaps due to the poor execution of these transcript modulation exhibiting remarkable repression of photosynthesis related genes resulting in chlorosis of leaves followed by penalty in crop yield. Thus, the present findings revealed an insight on the molecular warfare during host-virus interaction suggesting plausible signaling mechanisms and key biochemical pathways overriding MYMIV invasion in resistant genotype of V. mungo. In addition to inflate the existing knowledge base, the genomic resources identified in this orphan crop would be useful for integrating MYMIV-tolerance trait in susceptible cultivars of V. mungo.

No MeSH data available.


Related in: MedlinePlus