Analysis of alternative transcripts of the flaxL6rust resistance gene

Ayliffe, Michael; Frost, Donna; Finnegan, E. Jean; Lawrence, Gregory J.; Anderson, Peter; Ellis, Jeffery G.

doi:10.1046/j.1365-313x.1999.00377.x

Cited by 82 publications

(66 citation statements)

References 18 publications

(34 reference statements)

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“…This finding suggests that the encoded protein products from these transcripts play a role in disease resistance. Our results from the N-TMV system indicate that the alternative N L transcript and presumably the encoded truncated N tr protein product have important roles in TMV resistance, which contrasts with the results published for L 6 flax resistance (9). Transgenic flax plants with an L 6 synthetic construct that fails to produce alternative transcripts induces a resistance response to rust that is similar to wild-type L 6 -containing plants.…”

Section: Discussioncontrasting

confidence: 94%

Alternatively spliced N resistance gene transcripts: Their possible role in tobacco mosaic virus resistance

Dinesh‐Kumar

Baker

2000

Proc. Natl. Acad. Sci. U.S.A.

327

226

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The N gene, a member of the Toll-IL-1 homology region-nucleotide binding site-leucine-rich repeat region (LRR) class of plant resistance genes, encodes two transcripts, N S and NL, via alternative splicing of the alternative exon present in the intron III. The NS transcript, predicted to encode the full-length N protein containing the Toll-IL-1 homology region, nucleotide binding site, and LRR, is more prevalent before and for 3 hr after tobacco mosaic virus (TMV) infection. The NL transcript, predicted to encode a truncated N protein (N tr ) lacking 13 of the 14 repeats of the LRR, is more prevalent 4 -8 hr after TMV infection. Plants harboring a cDNA-NS transgene, capable of encoding an N protein but not an N tr protein, fail to exhibit complete resistance to TMV. Transgenic plants containing a cDNA-NS-bearing intron III and containing 3 Ngenomic sequences, encoding both N S and NL transcripts, exhibit complete resistance to TMV. These results suggest that both N transcripts and presumably their encoded protein products are necessary to confer complete resistance to TMV.

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Section: Discussioncontrasting

confidence: 94%

Alternatively spliced N resistance gene transcripts: Their possible role in tobacco mosaic virus resistance

Dinesh‐Kumar

Baker

2000

Proc. Natl. Acad. Sci. U.S.A.

327

226

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“…In addition, many splice variants and loci encoding LRR truncations in the genome do not demonstrate constitutive activity [47][48][49][50][51][52] . Furthermore, some full-length plant NBS-LRR proteins, such as Rx and RPS2, are constitutively active when overexpressed in plant cells, suggesting that the LRR domain is not sufficient to inhibit autoactivation in those conditions 14,38,40 .…”

Section: The Lrr As a Regulatory Domainmentioning

confidence: 99%

Plant NBS-LRR proteins in pathogen sensing and host defense

2006

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Plant proteins belonging to the nucleotide-binding site-leucine-rich repeat (NBS-LRR) family are used for pathogen detection. Like the mammalian Nod-LRR protein 'sensors' that detect intracellular conserved pathogen-associated molecular patterns, plant NBS-LRR proteins detect pathogen-associated proteins, most often the effector molecules of pathogens responsible for virulence. Many virulence proteins are detected indirectly by plant NBS-LRR proteins from modifications the virulence proteins inflict on host target proteins. However, some NBS-LRR proteins directly bind pathogen proteins. Association with either a modified host protein or a pathogen protein leads to conformational changes in the amino-terminal and LRR domains of plant NBS-LRR proteins. Such conformational alterations are thought to promote the exchange of ADP for ATP by the NBS domain, which activates 'downstream' signaling, by an unknown mechanism, leading to pathogen resistance.Plants lack the adaptive immunity that vertebrates rely on to respond to pathogens. To successfully detect and ward off pathogens, plants must rely solely on genes stably encoded in the genome. Although the exact mechanisms of pathogen detection differ, plants, like animals, use two distinct defense 'systems' to recognize and respond to pathogen challenge 1 . Pathogen-associated molecular patterns (PAMPs), such as bacterial flagellin, lipopolysaccharides and fungal-oomycete cellulose-binding elicitor proteins, are recognized by plant transmembrane receptors that activate basal defense, a first line of defense against pathogens that is reminiscent of innate immunity in vertebrates 2, 3. In both plants and animals, it is hypothesized that a biological 'arms race' is occurring, in which pathogens have acquired mechanisms to evade PAMP-triggered immunity by evolving effector molecules that modify the state of the host cell, thereby bypassing or disrupting the first line of defense. Plant evolution has countered with proteins that detect specific effector molecules, a mechanism called 'effector-triggered immunity'1 that amounts to a second line of defense. Plant effector-triggered immunity is more akin to mammalian adaptive immunity in that pathogen effectors, rather than conserved elements such as PAMPs, are specifically recognized. However, unlike the situation in mammalian adaptive immunity, the plant host specificity determinants of effector-triggered immunity are encoded in every cell of an organism.The genes encoding the specificity determinants of effector-triggered immunity are known as resistance (R) genes. Most R genes encode proteins that contain a nucleotide-binding site (NBS) and leucine-rich repeats (LRRs). NBS-LRR proteins are involved in the recognition of specialized pathogen effectors (also called avirulence (Avr) proteins) that are thought to provide virulence function in the absence of the cognate R gene 1 . NBS-LRR proteins are also important in animal innate immune systems; however, in animals they seem to be involved in PAMP recognition rather th...

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“…Alternative splicing for TIR-NB-LRR genes, N, L6, RPS4, and Y-1, a gene for resistance to potato virus Y, has been reported (Ayliffe et al 1999;Dinesh-Kumar and Baker 2000;Jordan et al 2002;Lawrence et al 1995;Vidal et al 2002). In the case of RAC1, amplification of the transcript by gene-specific primers revealed a copy of RAC1 transcript that retained intron 1.…”

Section: Discussionmentioning

confidence: 99%

The Arabidopsis TIR-NB-LRR Gene RAC1 Confers Resistance to Albugo candida (White Rust) and Is Dependent on EDS1 but not PAD4

Borhan¹,

Holub²,

Beynon³

et al. 2004

MPMI

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Resistance to Albugo candida isolate Acem1 is conferred by a dominant gene, RAC1, in accession Ksk-1 of Arabidopsis thaliana. This gene was isolated by positional cloning and is a member of the Drosophila toll and mammalian interleukin-1 receptor (TIR) nucleotide-binding site leucine-rich repeat (NB-LRR) class of plant resistance genes. Strong identity of the TIR and NB domains was observed between the predicted proteins encoded by the Ksk-1 allele and the allele from an Acem1-susceptible accession Columbia (Col) (99 and 98%, respectively). However, major differences between the two predicted proteins occur within the LRR domain and mainly are confined to the β-strand/β-turn structure of the LRR. Both proteins contain 14 imperfect repeats. RAC1-mediated resistance was analyzed further using mutations in defense regulation, including: pad4-1, eds1-1, and NahG, in the presence of the RAC1 allele from Ksk-1. White rust resistance was completely abolished by eds1-1 but was not affected by either pad4-1 or NahG.

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Analysis of alternative transcripts of the flaxL6rust resistance gene

Cited by 82 publications

References 18 publications

Alternatively spliced N resistance gene transcripts: Their possible role in tobacco mosaic virus resistance

Alternatively spliced N resistance gene transcripts: Their possible role in tobacco mosaic virus resistance

Plant NBS-LRR proteins in pathogen sensing and host defense

The Arabidopsis TIR-NB-LRR Gene RAC1 Confers Resistance to Albugo candida (White Rust) and Is Dependent on EDS1 but not PAD4

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