The Arabidopsis gene SCI2 encodes a RNA-binding protein which regulates the suppression of plant response to abiotic stress

Lead Research Organisation: University of East Anglia
Department Name: Biological Sciences


Our agriculture focuses on the production of crops that will feed us and our animals. However, these crops are attractive food for the myriad of herbivore insects and nematodes that also wish to eat them. It is not generally known that plants are extraordinarily sophisticated organisms: although they may appear to unresponsive, they constantly monitor themselves and their environment, and when they sense they have been attacked by insect pests or pathogens, or exposed to an abiotic stress such as drought or salinity, they respond rapidly to defend themselves. These defence responses are not only physical, but also chemical. The chemical response is based on the fact that plants are the masters of synthetic organic chemistry: in response to attack by pests they synthesise a variety of toxic compounds that include volatile terpenes, and toxic alkaloids, phenolics, and flavonoids. The production of these compounds deters all but the most determined, or well-defended, of insects. An unexpected corollary is that because the early selection and breeding of our crop plants deliberately produced varieties that lacked the bitter flavours many of these compounds cause, our domesticated varieties have therefore also been bred, unintentionally, to be vulnerable to pests. Other important factors that reduce yield include drought, salinity, and mechanical damage. Research in my laboratory has shown that plant response to pests has many similarities to plant response to drought, salinity, and to mechanical damage: that is, there are common features in the ways in which plants respond to these stresses. We wish to understand how the plant detect the stress, and then converts this signal to induce a response that adapts the plant to resist that stress. We have shown that when plants are wounded by insects, or are subject to stress, they make a compound called jasmonate, which appears to travel through the plant and induce a signal pathway that induces responses to stress, including the production of secondary chemical products. We have identified a number of genes that regulate the jasmonate signal pathway. This project is to characterise a new component of this pathway we recently discovered, called SCI2. When SCI2 is mutated the plant has greatly enhanced response to wounding and to stress, and greatly enhanced resistance. This means that the normal function of SCI2 is to suppress these responses. Therefore, the stress response pathway includes both activators and suppressers of the response. Because the synthesis of SCI2 is itself activated by jasmonate, this indicates that the jasmonate signal activates a suppresser of the jasmonate response pathway. We suspect that such a mechanism could assist in regulating the tissue-specificity of plant response to jasmonate. SCI2 is a protein predicted to bind to RNA products of other genes. We anticipate therefore that SCI2 will function by regulating the processing of these RNAs, by enchancing or reducing their stability. Therefore we shall identify the RNAs that bind SCI2, determine whether the level of the SCI2 protein affects the stability of these RNAs, and discover how expression of the SCI2 gene is regulated, and what gene expression SCI2 regulates.

Technical Summary

The jasmonate (JA) signal pathway regulates plant response to both biotic and to abiotic stress. It connects perception of the stress to the execution of the response. In the first part of this pathway, perception of the stress leads to the synthesis of JAs; in the second part, perception of Jas leads to the execution of the response. We are concerned with the processes by which JAs are perceived, and JA responses are induced. Our preliminary work led to the isolation and cloning of a gene we named COI1 which was required for the JA perception-response pathway. coi1 mutants lacked responses to abiotic and biotic stresses, and were generally unable to survive drought, pest infestation, and pathogen attack. We isolated suppresser mutations that reverted coi1 to near-wild type. One such mutant, named sci2, was mapped genetically, and the gene was isolated and confirmed by stable complementation. The sci2 mutant is interesting because it is genetically recessive, but has greatly enhanced response to wounding, to JA, and has immunity to the pathogen Erysiphe cichoracearum through an induced hypersensitive reaction that involves the production of reactive oxygen at the penetration site, and induced resistance to insect pests. This indicates that SCI2 is a suppresser of the JA signal pathway that regulates response to abiotic stress and innate immunity. SCI2 has two significant features: it encodes a KH-domain protein predicted to function by regulating the processing of a set of RNA transcripts, and its transcription is regulated by abiotic stress, or JA. This latter appears counter-intuitive: the transcriptional activation of a gene which suppresses the signal pathway that activates its transcription. We propose to investigate SCI2 function by a combination of genetic, molecular genetic, biochemical, and physiological studies. We shall identify the RNA transcripts to which SCI2 binds, and through which its function is apparently expressed. We shall also test for binding of SCI2 to proteins in the JA pathway. We shall examine the transcriptional regulation of SCI2, and determine the genes whose transctiption is regulated by SCI2. These results will provide a platform for the understanding of the role of the KH-protein SCI2 in plant defence signalling. To our knowledge, no other groups in the UK are investigating these proteins in plants, and no others on the international scene are studying their role in stress signalling.


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