A family of genes including ETR1, ETR2, EIN4, ERS1, and ERS2 is implicated in ethylene perception in Arabidopsis thaliana. As only dominant mutations were previously available for these genes, it was unclear whether all of them are components in the ethylene signaling pathway and whether they code for positive or negative regulators of ethylene responses. In this study, we have isolated loss-of-function mutations of four of these genes (ETR1, ETR2, EIN4, and ERS2) and identified an ethylene-independent role of ETR1 in promoting cell elongation. Quadruple mutants had constitutive ethylene responses, revealing that these proteins negatively regulate ethylene responses and that the induction of ethylene response in Arabidopsis is through inactivation rather than activation of these proteins.
Plant growth homeostasis and defense responses are regulated by BONZAI1 (BON1), an evolutionarily conserved gene. Here, we show that growth regulation by BON1 is mediated through defense responses. BON1 is a negative regulator of a haplotype-specific Resistance (R) gene SNC1. The bon1-1 loss-of-function mutation activates SNC1, leading to constitutive defense responses and, consequently, reduced cell growth. In addition, a feedback amplification of the SNC1 gene involving salicylic acid is subject to temperature control, accounting for the regulation of growth and defense by temperature in bon1-1 and many other mutants. Thus, plant growth homeostasis involves the regulation of an R gene by BON1 and the intricate interplay between defense responses and temperature responses.
ERS (ethylene response sensor), a gene in the Arabidopsis thaliana ethylene hormone-response pathway, was uncovered by cross-hybridization with the Arabidopsis ETR1 gene. The deduced ERS protein has sequence similarity with the amino-terminal domain and putative histidine protein kinase domain of ETR1, but it does not have a receiver domain as found in ETR1. A missense mutation identical to the dominant etr1-4 mutation was introduced into the ERS gene. The altered ERS gene conferred dominant ethylene insensitivity to wild-type Arabidopsis. Double-mutant analysis indicates that ERS acts upstream of the CTR1 protein kinase gene in the ethylene-response pathway.
The plant hormone ethylene regulates a variety of processes of growth and development. To identify components in the ethylene signal transduction pathway, we screened for ethylene-insensitive mutants in Arabidopsis thaliana and isolated a dominant etr2-1 mutant. The etr2-1 mutation confers ethylene insensitivity in several processes, including etiolated seedling elongation, leaf expansion, and leaf senescence. Double mutant analysis indicates that ETR2 acts upstream of CTR1, which codes for a Raf-related protein kinase. We cloned the ETR2 gene on the basis of its map position, and we found that it exhibits sequence homology to the ethylene receptor gene ETR1 and the ETR1-like ERS gene. ETR2 may thus encode a third ethylene receptor in Arabidopsis, transducing the hormonal signal through its ''twocomponent'' structure. Expression studies show that ETR2 is ubiquitously expressed and has a higher expression in some tissues, including inf lorescence and f loral meristems, petals, and ovules.
The Rex protein of human T-cell leukemia virus type 1, like the functionally equivalent Rev protein of human immunodeficiency virus type 1, contains a leucine-rich activation domain that specifically interacts with the human nucleoporin-like Rab/hRIP cofactor. Here, this Rex sequence is shown to function also as a protein nuclear export signal (NES). Rex sequence libraries containing randomized forms of the activation domain/ NES were screened for retention of the ability to bind Rab/hRIP by using the yeast two-hybrid assay. While the selected sequences differed widely in primary sequence, all were functional as Rex activation domains. In contrast, randomized sequences that failed to bind Rab/hRIP lacked Rex activity. The selected sequences included one with homology to the Rev activation domain/NES and a second that was similar to the NES found in the cellular protein kinase inhibitor ␣. A highly variant, yet fully active, activation domain sequence selected on the basis of Rab/hRIP binding retained full NES function even though this sequence preserved only a single leucine residue. In contrast, nonfunctional activation domain mutants that were unable to bind Rab/hRIP had also lost NES function. These data demonstrate that NES activity is a defining characteristic of the activation domains found in the Rev/Rex class of retroviral regulatory proteins and strongly support the hypothesis that the Rab/hRIP cofactor plays a critical role in mediating the biological activity of these NESs. In addition, these data suggest a consensus sequence for NESs of the Rev/Rex class.The pathogenic complex retroviruses human T-cell leukemia virus type 1 (HTLV-1) and human immunodeficiency virus type 1 (HIV-1) belong to distinct retroviral families and display little sequence homology. The approaches used by these viruses to regulate proviral gene expression are nevertheless remarkably similar (reviewed in reference 5). Thus, each virus encodes a transcriptional regulatory protein that acts on the respective viral long terminal repeat promoter element to dramatically enhance viral gene expression. In addition, each virus also encodes an essential posttranscriptional regulatory protein, termed Rex in HTLV-1 and Rev in HIV-1, that induces the sequence-specific nuclear export, and hence translation, of the incompletely spliced viral mRNA species that encode the various viral structural proteins (8,11,16,17,20,23,27).Initial evidence favoring the hypothesis that Rex and Rev, despite lacking any significant sequence identity, might nevertheless mediate the nuclear export of target RNAs via the same mechanism came from the finding that Rex could partly rescue the replication of a Rev-deficient HIV-1 provirus (36). Subsequently, both Rev and Rex were shown to bind directly to structured RNA response elements present in their target RNAs (3,6,14,19,29,38,41) and to contain multimerization domains that are essential for the recruitment of additional Rev or Rex molecules (Fig. 1) (2, 26, 34). In addition, both Rev and Rex contain short, leu...
An elevated growth temperature often inhibits plant defense responses and renders plants more susceptible to pathogens. However, the molecular mechanisms underlying this modulation are unknown. To genetically dissect this regulation, we isolated mutants that retain disease resistance at a higher growth temperature in Arabidopsis. One such heat-stable mutant results from a point mutation in SNC1, a NB-LRR encoding gene similar to disease resistance (R) genes. Similar mutations introduced into a tobacco R gene, N, confer defense responses at elevated temperature. Thus R genes or R-like genes involved in recognition of pathogen effectors are likely the causal temperature-sensitive component in defense responses. This is further supported by snc1 intragenic suppressors that regained temperature sensitivity in defense responses. In addition, the SNC1 and N proteins had a reduction of nuclear accumulation at elevated temperature, which likely contributes to the inhibition of defense responses. These findings identify a plant temperature sensitive component in disease resistance and provide a potential means to generate plants adapting to a broader temperature range.
Plant-pathogen interactions are known to be affected by environmental factors including temperature; however, the temperature effects have not been systematically studied in plant disease resistance. Here, we characterized the effects of a moderate increase in temperature on resistance to bacterial pathogen Pseudomonas syringae and two viral elicitors in Arabidopsis thaliana and Nicotiana benthamiana. Both the basal and the resistance (R) gene-mediated defense responses to Pseudomonas syringae are found to be inhibited by a moderately high temperature, and hypersensitive responses induced by R genes against two viruses are also reduced by an increase of temperature. These indicate that temperature modulation of defense responses to biotrophic and hemibiotrophic pathogens might be a general phenomenon. We further investigated the roles of two small signaling molecules, salicylic acid and jasmonic acid, as well as two defense regulators, EDS1 and PAD4, in this temperature modulation. These components, though modulated by temperature or involved in temperature regulation or both, are not themselves determinants of temperature sensitivity in the defense responses analyzed. The inhibition of plant defense response by a moderately high temperature may thus be mediated by other defense signaling components or a combination of multiple factors.
Wild-type Arabidopsis plants maintain a relatively constant size over a wide range of temperatures. Here we show that this homeostasis requires the BONZAI1 (BON1) gene because bon1 null mutants make miniature fertile plants at 22°C but have wild-type appearance at 28°C. The expression of BON1 and a BON1-associated protein (BAP1) is modulated by temperature. Thus BON1 and BAP1 may have a direct role in regulating cell expansion and cell division at lower temperatures. BON1 contains a Ca 2+ -dependent phospholipid-binding domain and is associated with the plasma membrane. It belongs to the copine gene family, which is conserved from protozoa to humans. Our data suggest that this gene family may function in the pathway of membrane trafficking in response to external conditions. Multicellular organisms develop and maintain a relatively constant size and shape over a wide range of different environmental conditions. This homeostasis is accomplished both by extrinsic mechanisms (e.g., movements that can reestablish a constant environment) and by intrinsic mechanisms that alter cellular metabolism so that the organism can retain its morphology despite the altered environment. Animals can move to a new environment to maintain constant external conditions; whereas plants are anchored and can only bend in response to changes in environmental factors such as light, gravity, and mechanical force.The existence of intrinsic homeostatic mechanisms suggests genetic control, which could be revealed by mutants that fail to maintain constant size and shape in response to an environmental perturbation. Recently, a genetic pathway has been discovered in Drosophila that regulates cell, organ, and body size. Mutations in genes apparently functioning in the insulin-signaling pathway result in miniature flies comprised of smaller and fewer cells (Oldham et al. 2000) under conditions where wild type maintains its standard size. These mutant flies phenocopy those wild type under starvation or overcrowding, which reveals a link between the control of morphology and nutritional conditions in the environment.For plants these intrinsic genetic mechanisms must be essential in temperature homeostasis because these organisms are sessile and do not maintain constant body temperatures when the ambient temperature changes. Indeed, most plants maintain a relatively constant phenotype in varied temperatures. For example, Arabidopsis grows to similar size and morphology (less than a twofold change) over temperatures that range from 16°C to 30°C. This suggests the existence of genes whose function is to permit adaptation to temperature variation.Studies on the tolerance of plants to freezing have revealed the mechanisms that contribute to survival at very low temperatures. Both physiological and genetic analyses point to the membrane systems as key to this homeostasis. Extreme cold results in the disruption of membrane function and death (Steponkus 1984). Plants can increase their tolerance to extreme cold by previous exposure to low nonfreezing temper...
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