“…Some of the lesions occur independently of SA, while others require elevated levels of SA (Hunt et al, 1997;Weymann et al, 1995). The wildtype copies of the mutated genes had been thought to be involved in the genetic control of the HR response (Dietrich et al, 1994;Greenberg and Ausubel, 1993). However, identi®cation of some of these genes has revealed that the perturbance of normal metabolic pathways that seem unrelated to defense reactions may also result in formation of necrotic lesions (Hu et al, 1998;Mach et al, 2001).…”
Summary
Thionins are a group of antimicrobial polypeptides that form part of the plant's defense mechanism against pathogens. The Thi 2.1 thionin gene of Arabidopsis thaliana has been shown to be inducible by jasmonic acid (JA), an oxylipin‐like hormone derived from oxygenated linolenic acid and synthesized via the octadecanoid pathway. The JA‐dependent regulation of the Thi 2.1 gene has been exploited for setting up a genetic screen for the isolation of signal transduction mutants that constitutively express the Thi 2.1 gene. Ten cet‐mutants have been isolated which showed a constitutive expression of the thionin gene. Allelism tests revealed that they represent at least five different loci. Some mutants are dominant, others recessive, but all cet mutations behaved as monogenic traits when backcrossed with Thi 2.1‐GUS plants. Some of the mutants overproduce JA and its bioactive precursor 12‐oxophytodienoic acid (OPDA) up to 40‐fold while others have the same low levels as the control wildtype plants. Two of the mutants showed a strong induction of both the salicylic acid (SA)‐ and the JA‐dependent signaling pathways, while the majority seems to be affected only in the octadecanoid pathway. The Thi 2.1 thionin gene and the Pdf 1.2 defensin gene are activated independently, though both are regulated by JA. The cet‐mutants, except for one, also show a spontaneous leaf cell necrosis, a reaction often associated with the systemic acquired resistance (SAR) pathway.
“…Some of the lesions occur independently of SA, while others require elevated levels of SA (Hunt et al, 1997;Weymann et al, 1995). The wildtype copies of the mutated genes had been thought to be involved in the genetic control of the HR response (Dietrich et al, 1994;Greenberg and Ausubel, 1993). However, identi®cation of some of these genes has revealed that the perturbance of normal metabolic pathways that seem unrelated to defense reactions may also result in formation of necrotic lesions (Hu et al, 1998;Mach et al, 2001).…”
Summary
Thionins are a group of antimicrobial polypeptides that form part of the plant's defense mechanism against pathogens. The Thi 2.1 thionin gene of Arabidopsis thaliana has been shown to be inducible by jasmonic acid (JA), an oxylipin‐like hormone derived from oxygenated linolenic acid and synthesized via the octadecanoid pathway. The JA‐dependent regulation of the Thi 2.1 gene has been exploited for setting up a genetic screen for the isolation of signal transduction mutants that constitutively express the Thi 2.1 gene. Ten cet‐mutants have been isolated which showed a constitutive expression of the thionin gene. Allelism tests revealed that they represent at least five different loci. Some mutants are dominant, others recessive, but all cet mutations behaved as monogenic traits when backcrossed with Thi 2.1‐GUS plants. Some of the mutants overproduce JA and its bioactive precursor 12‐oxophytodienoic acid (OPDA) up to 40‐fold while others have the same low levels as the control wildtype plants. Two of the mutants showed a strong induction of both the salicylic acid (SA)‐ and the JA‐dependent signaling pathways, while the majority seems to be affected only in the octadecanoid pathway. The Thi 2.1 thionin gene and the Pdf 1.2 defensin gene are activated independently, though both are regulated by JA. The cet‐mutants, except for one, also show a spontaneous leaf cell necrosis, a reaction often associated with the systemic acquired resistance (SAR) pathway.
“…These phenotypes are highly similar to those of Arabidopsis mutants such as acd1 (accelerated cell death), cpr1 (constitutive expressor of PR genes), lsd1 (lesion stimulating disease 1), and agd2 (aberrant growth and death 2), which display a constitutive pathogen response. [44][45][46][47] Untransformed wild-type, vector control, and CDD I575S transgenic plants grown under identical conditions did not show these phenotypes (Figure 9). CDD and CDD I157S proteins were detected immunologically in transgenic lines transformed with CDD and CDD I157S constructs.…”
Section: Induction Of Cell Death By Atbag6 In Arabidopsis Plantmentioning
confidence: 95%
“…46,48 To determine whether the cell death (Figure 9c) found in transgenic lines expressing CDD involved HR-like lesions, plants were stained for callose with aniline blue and observed under fluorescence microscopy ( Figure 9d). Whole-mount leaves of CDD transgenic plants showed prominent abundance of callose, whereas wild-type, control, and CDD I575S transgenic plants did not (Figure 9d).…”
Section: Induction Of Cell Death By Atbag6 In Arabidopsis Plantmentioning
Calmodulin (CaM) influences many cellular processes by interacting with various proteins. Here, we isolated AtBAG6, an Arabidopsis CaM-binding protein that contains a central BCL-2-associated athanogene (BAG) domain. In yeast and plants, overexpression of AtBAG6 induced cell death phenotypes consistent with programmed cell death (PCD). Recombinant AtBAG6 had higher affinity for CaM in the absence of free Ca 2 þ than in its presence. An IQ motif (IQXXXRGXXXR, where X denotes any amino-acid) was required for Ca 2 þ -independent CaM complex formation and single amino-acid changes within this motif abrogated both AtBAG6-activated CaM-binding and cell death in yeast and plants. A 134-amino-acid stretch, encompassing both the IQ motif and BAG domain, was sufficient to induce cell death. Agents generating oxygen radicals, which are known to be involved in plant PCD, specifically induced the AtBAG6 transcript. Collectively, these results suggest that AtBAG6 is a stress-upregulated CaM-binding protein involved in plant PCD.
“…Following inoculation plants were covered to maintain high humidity and placed in a Percival growth chamber. Seven to 10 days after inoculation plants were assayed for resistance by viewing under a dissecting microscope to score development of conidiophores (Dietrich et aL, 1994) followed by lactophenoltrypan blue staining of individual leaves to observe fungal development within the leaf tissue (Keogh et al, 1980).…”
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