Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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) discriminating self- and non-self pollen is regulated by S-locus genes in Brassica. In most of the S haplotypes, a highly polymorphic S-locus glycoprotein ( SLG) gene is tightly linked to genes for the SI determinants, S-receptor kinase ( SRK) and SP11, although the precise function of SLG in SI has not been clarified. In the present study, we performed DNA gel blot analysis for S(32), S(33), and S(36) haplotypes of Brassica rapa showing normal SI phenotypes and concluded that there might be no SLG in their genome. RNA gel blot analysis of the SLG-less S haplotypes indicated the possible existence of eSRK transcripts in the stigma. These three S haplotypes are useful resources to discern the molecular mechanism of the SI reaction without SLG.
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PMID:The S haplotypes lacking SLG in the genome of Brassica rapa. 1278 10

Self-incompatibility (SI) response in Brassica is initiated by haplotype-specific interactions between the pollen-borne ligand S locus protein 11/SCR and its stigmatic S receptor kinase, SRK. This binding induces autophosphorylation of SRK, which is then thought to trigger a signaling cascade that leads to self-pollen rejection. A recessive mutation of the modifier (m) gene eliminates the SI response in stigma. Positional cloning of M has revealed that it encodes a membrane-anchored cytoplasmic serine/threonine protein kinase, designated M locus protein kinase (MLPK). Transient expression of MLPK restores the ability of mm papilla cells to reject self-pollen, suggesting that MLPK is a positive mediator of Brassica SI signaling.
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PMID:A membrane-anchored protein kinase involved in Brassica self-incompatibility signaling. 1500 63

In Brassica , the thioredoxin h proteins, THL1 and THL2, were previously found to be potential inhibitors of the S receptor kinase (SRK) in the Brassica self-incompatibility response. To investigate the biological roles of THL1 and THL2 in pollen-pistil interactions, the stigma-specific SLR1 promoter was used to drive antisense THL1/2 expression in Brassica napus cv. Westar. This cultivar is normally compatible, but antisense suppression of THL1/2 led to a low level constitutive rejection of all Brassica napus pollen tested. Fluorescence microscopy revealed that the pollen rejection was a typical Brassica self-incompatibility rejection response with reduced pollen adhesion, germination and pollen tube growth. In addition, Westar was found to express the SLG(15) and SRK(15) proteins which may be the target of regulation by THL1 and THL2. Thus, these results indicate that the THL1 and THL2 are required for full pollen acceptance in B. napus cv. Westar.
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PMID:Antisense suppression of thioredoxin h mRNA in Brassica napus cv. Westar pistils causes a low level constitutive pollen rejection response. 1560 5

Sexual reproduction in many flowering plants involves self-incompatibility (SI), which is one of the most important systems to prevent inbreeding. In many species, the self-/nonself-recognition of SI is controlled by a single polymorphic locus, the S-locus. Molecular dissection of the S-locus revealed that SI represents not one system, but a collection of divergent mechanisms. Here, we discuss recent advances in the understanding of three distinct SI mechanisms, each controlled by two separate determinant genes at the S-locus. In the Brassicaceae, the determinant genes encode a pollen ligand and its stigmatic receptor kinase; their interaction induces incompatible signaling(s) within the stigma papilla cells. In the Solanaceae-type SI, the determinants are a ribonuclease and an F-box protein, suggesting the involvement of RNA and protein degradation in the system. In the Papaveraceae, the only identified female determinant induces a Ca2+-dependent signaling network that ultimately results in the death of incompatible pollen.
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PMID:Self-incompatibility in plants. 1586 4

The highly polymorphic S-locus receptor kinase (SRK) is the stigma determinant of specificity in the self-incompatibility response of the Brassicaceae. SRK spans the plasma membrane of stigma epidermal cells, and it is activated in an allele-specific manner on binding of its extracellular region (eSRK) to its cognate pollen coat-localized S-locus cysteine-rich (SCR) ligand. SRK, like several other receptor kinases, forms dimers in the absence of ligand. To identify domains in SRK that mediate ligand-independent dimerization, we assayed eSRK for self-interaction in yeast. We show that SRK dimerization is mediated by two regions in eSRK, primarily by a C-terminal region inferred by homology modeling/fold recognition techniques to assume a PAN_APPLE-like structure, and secondarily by a region containing a signature sequence of the S-domain gene family, which might assume an EGF-like structure. We also show that eSRK exhibits a marked preference for homodimerization over heterodimerization with other eSRK variants and that this preference is mediated by a small, highly variable region within the PAN_APPLE domain. Thus, the extensive polymorphism exhibited by the eSRK not only determines differential affinity toward the SCR ligand, as has been assumed thus far, but also underlies a previously unrecognized allelic specificity in SRK dimerization. We propose that preference for SRK homodimerization explains the codominance exhibited by a majority of SRKs in the typically heterozygous stigmas of self-incompatible plants, whereas an increased propensity for heterodimerization combined with reduced affinity of heterodimers for cognate SCRs might underlie the dominant-recessive or mutual weakening relationships exhibited by some SRK allelic pairs.
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PMID:Structural modules for receptor dimerization in the S-locus receptor kinase extracellular domain. 1760 67

Brassica self-incompatibility, a highly discriminating outbreeding mechanism, has become a paradigm for the study of plant cell-cell communications. When self-pollen lands on a stigma, the male ligand S cysteine-rich (SCR), which is present in the pollen coat, is transmitted to the female receptor, S-locus receptor kinase (SRK). SRK is a membrane-spanning serine/threonine receptor kinase present in the stigmatic papillar cell membrane. Haplotype-specific binding of SCR to SRK brings about pollen rejection. The extracellular receptor domain of SRK (eSRK) is responsible for binding SCR. Based on sequence homology, eSRK can be divided into three subdomains: B lectin-like, hypervariable, and PAN. Biochemical analysis of these subdomains showed that the hypervariable subdomain is responsible for most of the SCR binding capacity of eSRK, whereas the B lectin-like and PAN domains have little, if any, affinity for SCR. Fine mapping of the SCR binding region of SRK using a peptide array revealed a region of the hypervariable subdomain that plays a key role in binding the SCR molecule. We show that residues within the hypervariable subdomain define SRK binding and are likely to be involved in defining haplotype specificity.
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PMID:S cysteine-rich (SCR) binding domain analysis of the Brassica self-incompatibility S-locus receptor kinase. 1768 75

A common yet poorly understood evolutionary transition among flowering plants is a switch from outbreeding to an inbreeding mode of mating. The model plant Arabidopsis thaliana evolved to an inbreeding state through the loss of self-incompatibility, a pollen-rejection system in which pollen recognition by the stigma is determined by tightly linked and co-evolving alleles of the S-locus receptor kinase (SRK) and its S-locus cysteine-rich ligand (SCR). Transformation of A. thaliana, with a functional AlSRKb-SCRb gene pair from its outcrossing relative A. lyrata, demonstrated that A. thaliana accessions harbor different sets of cryptic self-fertility-promoting mutations, not only in S-locus genes, but also in other loci required for self-incompatibility. However, it is still not known how many times and in what manner the switch to self-fertility occurred in the A. thaliana lineage. Here, we report on our identification of four accessions that are reverted to full self-incompatibility by transformation with AlSRKb-SCRb, bringing to five the number of accessions in which self-fertility is due to, and was likely caused by, S-locus inactivation. Analysis of S-haplotype organization reveals that inter-haplotypic recombination events, rearrangements, and deletions have restructured the S locus and its genes in these accessions. We also perform a Quantitative Trait Loci (QTL) analysis to identify modifier loci associated with self-fertility in the Col-0 reference accession, which cannot be reverted to full self-incompatibility. Our results indicate that the transition to inbreeding occurred by at least two, and possibly more, independent S-locus mutations, and identify a novel unstable modifier locus that contributes to self-fertility in Col-0.
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PMID:Independent S-locus mutations caused self-fertility in Arabidopsis thaliana. 1930 Apr 85

The self-incompatibility response of crucifers is a barrier to fertilization in which arrest of pollen tube development is mediated by allele-specific interactions between polymorphic receptors and ligands encoded by the S-locus haplotype. Activation of stigma-expressed S-locus receptor kinase (SRK) [1] by pollen coat-localized S-locus cysteine-rich (SCR) ligand [2-5] and the resulting rejection of pollen occurs only if receptor and ligand are encoded by the same S haplotype [4, 6-8]. To identify residues within the SRK extracellular domain (eSRK) that are required for its ligand-selective activation, we assayed chimeric receptors and receptor variants containing substitutions at polymorphic sites in Arabidopsis thaliana[9, 10]. We show that only a small number of the approximately 100 polymorphic residues in eSRK are required for ligand-specific activation of self-incompatibility in vivo. These essential residues occur in two noncontiguous clusters located at equivalent positions in the two variants tested. They also correspond to sites showing elevated levels of substitutions in other SRKs, suggesting that these residues could define self-incompatibility specificity in most SRKs. The results demonstrate that the majority of eSRK residues that show signals of positive selection and previously surmised to function as specificity determinants are not essential for specificity in the SRK-SCR interaction.
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PMID:In vivo detection of residues required for ligand-selective activation of the S-locus receptor in Arabidopsis. 1937 22

The coordinate evolution of self-incompatibility (SI) and stigma-anther separation, two mechanisms that promote cross-pollination in plants, has been a long-standing puzzle in evolution and development. Using a transgenic self-incompatible Arabidopsis thaliana model, we performed screens for mutants exhibiting a modified SI response. A mutation in the RNA-dependent RNA polymerase RDR6, which functions in trans-acting short interfering RNA (ta-siRNA) production, was found that simultaneously enhances SI and causes stigma exsertion, without associated increases in SRK transcript levels. While rdr6 mutants had been previously shown to exhibit stochastic stigma exsertion, our results demonstrate that the S-locus receptor kinase (SRK) gene further enhances pistil elongation and stigma exsertion in this mutant background, a process that requires SRK catalytic activity and correlates with SRK transcript levels. These results suggest that positive regulators or effectors of SI and pistil development are regulated by ta-siRNA(s). By establishing complex connections between SI and stigma exsertion through the sharing of a ta-siRNA-mediated regulatory pathway and the dual role of SRK in SI and pistil development, our study provides a molecular explanation for the coordinate evolution of these processes.
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PMID:A dual role for the S-locus receptor kinase in self-incompatibility and pistil development revealed by an Arabidopsis rdr6 mutation. 1976 57

Self-incompatibility (SI) has emerged as an evolutionary strategy to enhance the genetic variability of plant species. In Brassica, it is controlled by a single multiallelic locus, the S-locus, encoding a receptor kinase (SRK) expressed in the stigma papilla cells and its ligand, a small protein (SCR) located in the pollen coat. Pollen rejection is achieved only when the receptor recognizes SCR coming from the same S-allele. If a single papilla cell is simultaneously pollinated by a self- and a cross-pollen grain, it is capable of distinguishing between the two and responding accordingly, rejecting self while accepting cross pollen. This phenomenon reveals that SI response is strictly localized and does not involve the whole papilla cell. It also suggests that the distribution of SRK inside the cell may play an important role in regulating this dual response. We have recently demonstrated that SRK is mostly intracellular, only small amounts being present in distinct domains of the plasma membrane (PM), where interaction with SCR occurs. Following ligand recognition, the receptor-ligand complex is endocytosed and degraded. Based on this, we propose a model of the significance of SRK intracellular trafficking for the functioning and specificity of SI response.
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PMID:Brassica self-incompatibility: a glimpse below the surface. 1962 4


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