Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0277787 (stigma)
 13,352 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Self-incompatibility (SI) in Brassicaceae is sporophytically controlled by a single S-locus with multi allelic variety. The male S determinant, SP11/SCR (S-locus protein 11/S-locus cysteine-rich protein), is a small cysteine-rich protein, and the female S determinant, SRK (S-locus receptor kinase), functions as a receptor for SP11 at the surface of stigma papilla cells. Although a few of the following downstream factors in the SP11-SRK signaling cascade have been identified, a comprehensive understanding of the SI mechanism still remains unexplained in Brassicaceae. Analysis of self-compatible (SC) mutants is significant for understanding the molecular mechanism in SI reactions, thus we screened SC lines from a variety of Japanese bulk-populations of B. rapa vegetables. Two lines, TSC4 and TSC28, seem to have disruptions in the SI signaling cascade, while the other line, TSC2, seems to have a deficiency in a female S determinant, SRK. In TSC4 and TSC28, known SI-related factors, i.e. SRK, SP11, MLPK (M-locus protein kinase), THL (thioredoxin-h-like), and ARC1 (arm repeat containing 1), were expressed normally, and their expression levels were comparable with those in SI lines. On a B. rapa genetic linkage map, potential SC genes in TSC4 and TSC28 were mapped on linkage groups A3 and A1, respectively, whereas MLPK, ARC1, and THL were mapped on A3, A4, and A6, respectively. Although potential SC genes of TSC4 and MLPK were on the same linkage group, their positions were apparently independent. These results indicate that the SC genes of TSC4 and TSC28 are independent from the S-locus or known SI-related genes. Thus, the SC lines selected here have mutations in novel factors of the SI signaling cascade, and they will contribute to fill pieces in a signal transduction pathway of the SI system in Brassicaceae.
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PMID:Novel self-compatible lines of Brassica rapa L. isolated from the Japanese bulk-populations. 2055 95

The self-incompatibility (SI) response of the Brassicaceae is mediated by allele-specific interaction between the stigma-localized S-locus receptor kinase (SRK) and its ligand, the pollen coat-localized S-locus cysteine-rich protein (SCR). Based on work in Brassica spp., the thioredoxin h-like proteins THL1 and THL2, which interact with SRK, have been proposed to function as oxidoreductases that negatively regulate SRK catalytic activity. By preventing the spontaneous activation of SRK in the absence of SCR ligand, these thioredoxins are thought to be essential for the success of cross pollinations in self-incompatible plants. However, the in planta role of thioredoxins in the regulation of SI signaling has not been conclusively demonstrated. Here, we addressed this issue using Arabidopsis thaliana plants transformed with the SRKb-SCRb gene pair isolated from self-incompatible Arabidopsis lyrata. These plants express an intense SI response, allowing us to exploit the extensive tools and resources available in A. thaliana for analysis of SI signaling. To test the hypothesis that SRK is redox regulated by thioredoxin h, we expressed a mutant form of SRKb lacking a transmembrane-localized cysteine residue thought to be essential for the SRK-thioredoxin h interaction. We also analyzed transfer DNA insertion mutants in the A. thaliana orthologs of THL1 and THL2. In neither case did we observe an effect on the pollination responses of SRKb-expressing stigmas toward incompatible or compatible pollen. Our results are consistent with the conclusion that, contrary to their proposed role, thioredoxin h proteins are not required to prevent the spontaneous activation of SRK in the A. thaliana stigma.
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PMID:In planta assessment of the role of thioredoxin h proteins in the regulation of S-locus receptor kinase signaling in transgenic Arabidopsis. 2407 73

SRK (S-locus receptor kinase) is the receptor that allows stigma epidermal cells to discriminate between genetically related ('self') and genetically unrelated ('non-self') pollen in the self-incompatibility response of the Brassicaceae. SRK and its ligand, the pollen coat-localized SCR (S-locus cysteine-rich protein), are highly polymorphic, and their allele-specific interaction explains specificity in the self-incompatibility response. The present article reviews current knowledge of the role of SRK in the recognition and response phases of self-incompatibility, and highlights the new insights provided by analysis of a transgenic self-incompatible Arabidopsis thaliana model.
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PMID:S-locus receptor kinase signalling. 2464 37

Most wild plants and some crops of the Brassicaceae express self-incompatibility, which is a mechanism that allows stigmas to recognize and discriminate against "self" pollen, thus preventing self-fertilization and inbreeding. Self-incompatibility in this family is controlled by a single S locus containing two multiallelic genes that encode the stigma-expressed S-locus receptor kinase and its pollen coat-localized ligand, the S-locus cysteine-rich protein. Physical interaction between receptor and ligand encoded in the same S locus activates the receptor and triggers a signaling cascade that results in inhibition of "self" pollen. Sequence information for many S-locus haplotypes in Brassica species has spurred studies of dominance relationships between S haplotypes and of S-locus structure, as well as the development of methods for S genotyping. Furthermore, molecular genetic studies have begun to identify genes that encode putative components of the self-incompatibility signaling pathway. In parallel, standard genetic analysis and QTL analysis of the poorly understood interspecific incompatibility phenomenon have been initiated to identify genes responsible for the inhibition of pollen from other species by the stigma. Herewith, we review recent studies of self-incompatibility and interspecific incompatibility, and we propose a model in which a universal pollen-inhibition pathway is shared by these two incompatibility systems.
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PMID:Self-incompatibility in Brassicaceae crops: lessons for interspecific incompatibility. 2498 88

The S-locus receptor kinase SRK is a highly polymorphic transmembrane kinase of the stigma epidermis. Through allele-specific interaction with its pollen coat-localized ligand, the S-locus cysteine-rich protein SCR, SRK is responsible for recognition and inhibition of self pollen in the self-incompatibility response of the Brassicaceae. The SRK extracellular ligand binding domain contains several potential N-glycosylation sites that exhibit varying degrees of conservation among SRK variants. However, the glycosylation status and functional importance of these sites are currently unclear. We investigated this issue in transgenic Arabidopsis thaliana stigmas that express the Arabidopsis lyrata SRKb variant and exhibit an incompatible response toward SCRb-expressing pollen. Analysis of single- and multiple-glycosylation site mutations of SRKb demonstrated that, although five of six potential N-glycosylation sites in SRKb are glycosylated in stigmas, N-glycosylation is not important for SCRb-dependent activation of SRKb. Rather, N-glycosylation functions primarily to ensure the proper and efficient subcellular trafficking of SRK to the plasma membrane. The study provides insight into the function of a receptor that regulates a critical phase of the plant life cycle and represents a valuable addition to the limited information available on the contribution of N-glycosylation to the subcellular trafficking and function of plant receptor kinases.
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PMID:Site-specific N-glycosylation of the S-locus receptor kinase and its role in the self-incompatibility response of the brassicaceae. 2548 Mar 68

Self-incompatibility in the Brassicaceae is controlled by multiple haplotypes encoding the pollen ligand (S-locus protein 11, SP11, also known as S-locus cysteine-rich protein, SCR) and its stigmatic receptor (S-receptor kinase, SRK). A haplotype-specific interaction between SP11/SCR and SRK triggers the self-incompatibility response that leads to self-pollen rejection, but the signalling pathway remains largely unknown. Here we show that Ca(2+) influx into stigma papilla cells mediates self-incompatibility signalling. Using self-incompatible Arabidopsis thaliana expressing SP11/SCR and SRK, we found that self-pollination specifically induced an increase in cytoplasmic Ca(2+) ([Ca(2+)]cyt) in papilla cells. Direct application of SP11/SCR to the papilla cell protoplasts induced Ca(2+) increase, which was inhibited by D-(-)-2-amino-5-phosphonopentanoic acid (AP-5), a glutamate receptor channel blocker. An artificial increase in [Ca(2+)]cyt in papilla cells arrested wild-type (WT) pollen hydration. Treatment of papilla cells with AP-5 interfered with self-incompatibility, and Ca(2+) increase on the self-incompatibility response was reduced in the glutamate receptor-like channel (GLR) gene mutants. These results suggest that Ca(2+) influx mediated by GLR is the essential self-incompatibility response leading to self-pollen rejection.
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PMID:Calcium signalling mediates self-incompatibility response in the Brassicaceae. 2725 Jun 81

The sporophytic system of self-incompatibility is a widespread genetic phenomenon in plant species, promoting out-breeding and maintaining genetic diversity. This phenomenon is of commercial importance in hybrid breeding of Brassicaceae crops and is controlled by single S locus with multiple S haplotypes. The molecular genetic studies of Brassica 'S' locus has revealed the presence of three tightly linked loci viz. S-receptor kinase (SRK), S-locus cysteine-rich protein/S-locus protein 11 (SCR/SP11), and S-locus glycoprotein (SLG). On self-pollination, the allele-specific ligand-receptor interaction activates signal transduction in stigma papilla cells and leads to rejection of pollen tube on stigmatic surface. In addition, arm-repeat-containing protein 1 (ARC1), M-locus protein kinase (MLPK), kinase-associated protein phosphatase (KAPP), exocyst complex subunit (Exo70A1) etc. has been identified in Brassica crops and plays a key role in self-incompatibility signaling pathway. Furthermore, the cytoplasmic calcium (Ca2+) influx in papilla cells also mediates self-incompatibility response in Brassicaceae, but how this cytoplasmic Ca2+ influx triggers signal transduction to inhibit pollen hydration is still obscure. There are many other signaling components which are not well characterized yet. Much progress has been made in elucidating the downstream multiple pathways of Brassica self-incompatibility response. Hence, in this review, we have made an effort to describe the recent advances made on understanding the molecular aspects of genetic mechanism of self-incompatibility in Brassicaceae.
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PMID:Progress on deciphering the molecular aspects of cell-to-cell communication in Brassica self-incompatibility response. 3007 32

Self-incompatibility (SI) is a genetic mechanism that rejects self-pollen and thus prevents inbreeding in some hermaphroditic angiosperms. In the Brassicaceae, SI involves a pollen-stigma recognition system controlled by a single locus known as the S locus, which consists of two highly polymorphic genes that encode S-locus cysteine-rich protein (SCR) and S-receptor kinase (SRK). When self-pollen lands on the stigma, the S-haplotype-specific interaction between SCR and SRK triggers SI. Here, we show that the GATA transcription factor BnA5.ZML1 suppresses SI responses in Brassica napus and is induced after compatible pollination. The loss-of-function mutant bna5.zml1 displays reduced self-compatibility. In contrast, overexpression of BnA5.ZML1 in self-incompatible stigmas leads to a partial breakdown of SI responses, suggesting that BnA5.ZML1 is a stigmatic compatibility factor. Furthermore, the expression levels of SRK and ARC1 are up-regulated in bna5.zml1 mutants, and they are down-regulated in BnA5.ZML1 overexpressing lines. SRK affects the cellular localization of BnA5.ZML1 through direct protein-protein interaction. Overall, our findings highlight the fundamental role of BnA5.ZML1 in SI responses in B. napus, establishing a direct interaction between BnA5.ZML1 and SRK in this process.
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PMID:The Brassica napus GATA transcription factor BnA5.ZML1 is a stigma compatibility factor. 3202 17


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