Cloning of an Invertebrate GABA Receptor from the Cyclodiene Resistance Locus in Drosophila

Impulsivity is a complex trait that varies across healthy individuals, although when excessive, it is generally regarded as dysfunctional. Impulsive behavior may lead to initiation of drug addiction that interferes with inhibitory controls, which may in turn result in facilitation of the individual’s impulsive acts. Although environmental factors play a considerable role in impulsive behavior, a body of evidence collected in twin studies suggests that about 45% of the variance in impulsivity is accounted for by genetic factors. Genetic variants studied in association with impulsivity include those fortryptophan hydroxylase 1 and 2 (TPH1 and TPH2), the serotonintransporter (SERT), serotonin receptors, and genes of the monoamine metabolism pathway (e.g., monoamine oxidase A, MAOA). Other systems may also play a role in these behaviors, such as the dopaminergic system (the dopamine receptors DRD2, DRD3, and DRD4, and the dopamine transporter, DAT), the catecholaminergic system (catechol-O-methyltransferase, COMT), and the GABAergic system (GABAreceptor subunit alpha-1, GABRA1; GABA receptor subunit alpha-6, GABRA6; and GABA receptor subunit beta-1, GABRB1). Taking into account involvement of the hypothalamic-pituitary-adrenal (HPA) axis, the number of candidate genes implicated in impulsivity may be increased significantly and, therefore, may go far beyond those of serotonergic and dopaminergic systems. For a number of years, our group has conducted studies of the association of genes involved in the modulation of the stress-responsive HPA axis and several neurotransmitter systems, all involved in the pathophysiology of anxiety and depressive disorders, impulse control and compulsive disorders, with drug addiction. These genes include those of the opioid system: the mu- and kappa-opioid receptors (OPRM1 and OPRK1) and the nociceptin/orphaninFQ receptor (OPRL1); the serotonergic system: TPH1 and TPH2 and the serotonin receptor 1B (5THR1B); the catecholamine system: COMT; the HPA axis: themelanocortin receptor type 2 (MC2R or adrenocorticotropic hormone, ACTHR); and the cannabinoid system: the cannabinoid receptor type 1 (CNR1). In this chapter we will focus on these findings.

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Heterogeneous expression of GABA receptor‐like subunits LCCH3 and GRD reveals functional diversity of GABA receptors in the honeybee Apis mellifera

British Journal of Pharmacology ◽

10.1111/bph.15135 ◽

2020 ◽

Vol 177 (17) ◽

pp. 3924-3940

Author(s):

Christopher Henry ◽

Thierry Cens ◽

Pierre Charnet ◽

Catherine Cohen‐Solal ◽

Claude Collet ◽

...

Keyword(s):

Apis Mellifera ◽

Functional Diversity ◽

Gaba Receptors ◽

Gaba Receptor ◽

Heterogeneous Expression

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High resolution mapping and candidate gene identification of downy mildew race 16 resistance in spinach

BMC Genomics ◽

10.1186/s12864-021-07788-8 ◽

2021 ◽

Vol 22 (1) ◽

Author(s):

Gehendra Bhattarai ◽

Wei Yang ◽

Ainong Shi ◽

Chunda Feng ◽

Braham Dhillon ◽

...

Keyword(s):

Candidate Genes ◽

Downy Mildew ◽

Association Analysis ◽

Spinacia Oleracea ◽

Genotyping By Sequencing ◽

Significant Snps ◽

Snp Markers ◽

Resistance Locus ◽

Downy Mildew Resistance ◽

Mildew Resistance

Abstract Background Downy mildew, the most devastating disease of spinach (Spinacia oleracea L.), is caused by the oomycete Peronospora effusa [=P. farinosa f. sp. spinaciae]. The P. effusa shows race specificities to the resistant host and comprises 19 reported races and many novel isolates. Sixteen new P. effusa races were identified during the past three decades, and the new pathogen races are continually overcoming the genetic resistances used in commercial cultivars. A spinach breeding population derived from the cross between cultivars Whale and Lazio was inoculated with P. effusa race 16 in an environment-controlled facility; disease response was recorded and genotyped using genotyping by sequencing (GBS). The main objective of this study was to identify resistance-associated single nucleotide polymorphism (SNP) markers from the cultivar Whale against the P. effusa race 16. Results Association analysis conducted using GBS markers identified six significant SNPs (S3_658,306, S3_692697, S3_1050601, S3_1227787, S3_1227802, S3_1231197). The downy mildew resistance locus from cultivar Whale was mapped to a 0.57 Mb region on chromosome 3, including four disease resistance candidate genes (Spo12736, Spo12784, Spo12908, and Spo12821) within 2.69–11.28 Kb of the peak SNP. Conclusions Genomewide association analysis approach was used to map the P. effusa race 16 resistance loci and identify associated SNP markers and the candidate genes. The results from this study could be valuable in understanding the genetic basis of downy mildew resistance, and the SNP marker will be useful in spinach breeding to select resistant lines.

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Disruption of barley immunity to powdery mildew by an in-frame Lys-Leu deletion in the essential protein SGT1

Genetics ◽

10.1093/genetics/iyaa026 ◽

2020 ◽

Vol 217 (2) ◽

Cited By ~ 1

Author(s):

Antony V E Chapman ◽

Matthew Hunt ◽

Priyanka Surana ◽

Valeria Velásquez-Zapata ◽

Weihui Xu ◽

...

Keyword(s):

Powdery Mildew ◽

Fungal Pathogens ◽

Novel Mutation ◽

Exome Capture ◽

Resistance Locus ◽

Hordeum Vulgare L ◽

Powdery Mildew Fungus ◽

Pathogen Effectors ◽

Cell Processes ◽

Disease Resistances

Abstract Barley (Hordeum vulgare L.) Mla (Mildew resistance locus a) and its nucleotide-binding, leucine-rich-repeat receptor (NLR) orthologs protect many cereal crops from diseases caused by fungal pathogens. However, large segments of the Mla pathway and its mechanisms remain unknown. To further characterize the molecular interactions required for NLR-based immunity, we used fast-neutron mutagenesis to screen for plants compromised in MLA-mediated response to the powdery mildew fungus, Blumeria graminis f. sp. hordei. One variant, m11526, contained a novel mutation, designated rar3 (required for Mla6 resistance3), that abolishes race-specific resistance conditioned by the Mla6, Mla7, and Mla12 alleles, but does not compromise immunity mediated by Mla1, Mla9, Mla10, and Mla13. This is analogous to, but unique from, the differential requirement of Mla alleles for the co-chaperone Rar1 (required for Mla12 resistance1). We used bulked-segregant-exome capture and fine mapping to delineate the causal mutation to an in-frame Lys-Leu deletion within the SGS domain of SGT1 (Suppressor of G-two allele of Skp1, Sgt1ΔKL308–309), the structural region that interacts with MLA proteins. In nature, mutations to Sgt1 usually cause lethal phenotypes, but here we pinpoint a unique modification that delineates its requirement for some disease resistances, while unaffecting others as well as normal cell processes. Moreover, the data indicate that the requirement of SGT1 for resistance signaling by NLRs can be delimited to single sites on the protein. Further study could distinguish the regions by which pathogen effectors and host proteins interact with SGT1, facilitating precise editing of effector incompatible variants.

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QTL Mapping of Seedling and Adult Plant Resistance to Septoria Tritici Blotch in Winter Wheat cv. Mandub (Triticum aestivum L.)

Agronomy ◽

10.3390/agronomy11061108 ◽

2021 ◽

Vol 11 (6) ◽

pp. 1108

Author(s):

Dominika Piaskowska ◽

Urszula Piechota ◽

Magdalena Radecka-Janusik ◽

Paweł Czembor

Keyword(s):

Mapping Population ◽

Triticum Aestivum L ◽

Seedling Stage ◽

Septoria Tritici Blotch ◽

Septoria Tritici ◽

Adult Plant ◽

Resistance Locus ◽

Phenotypic Variance ◽

Breeding Programs ◽

Plant Stage

Septoria tritici blotch (STB) is one of the most devastating foliar diseases of wheat worldwide. Host resistance is the most economical and safest method of controlling the disease, and information on resistance loci is crucial for effective breeding for resistance programs. In this study we used a mapping population consisting of 126 doubled-haploid lines developed from a cross between the resistant cultivar Mandub and the susceptible cultivar Begra. Three monopycnidiospore isolates of Z. tritici with diverse pathogenicity were used to test the mapping population and parents’ STB resistance at the seedling stage (under a controlled environment) and adult plant stage (polytunnel). For both types of environments, the percentage leaf area covered by necrosis (NEC) and pycnidia (PYC) was determined. A linkage map comprising 5899 DArTSNP and silicoDArT markers was used for the quantitative trait loci (QTL) analysis. The analysis showed five resistance loci on chromosomes 1B, 2B and 5B, four of which were derived from cv. Mandub. The location of QTL detected in our study on chromosomes 1B and 5B may suggest a possible identity or close linkage with Stb2/Stb11/StbWW and Stb1 loci, respectively. QStb.ihar-2B.4 and QStb.ihar-2B.5 detected on chromosome 2B do not co-localize with any known Stb genes. QStb.ihar-2B.4 seems to be a new resistance locus with a moderate effect (explaining 29.3% of NEC and 31.4% of PYC), conferring resistance at the seedling stage. The phenotypic variance explained by QTL detected in cv. Mandub ranged from 11.9% to 70.0%, thus proving that it is a good STB resistance source and can potentially be utilized in breeding programs.

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Subcellular Localization and Complements of GABAA and GABAC Receptors on Bullfrog Retinal Bipolar Cells

Journal of Neurophysiology ◽

10.1152/jn.2000.84.2.666 ◽

2000 ◽

Vol 84 (2) ◽

pp. 666-676 ◽

Cited By ~ 37

Author(s):

Jiu-Lin Du ◽

Xiong-Li Yang

Keyword(s):

Subcellular Localization ◽

Receptor Antagonist ◽

Gaba Receptor ◽

Drug Application ◽

Bipolar Cells ◽

Visual Signals ◽

Receptor Subtypes ◽

Inner Retina ◽

Axon Terminals ◽

Retinal Bipolar Cells

γ-Aminobutyric acid (GABA) receptors on retinal bipolar cells (BCs) are highly relevant to spatial and temporal integration of visual signals in the outer and inner retina. In the present work, subcellular localization and complements of GABAA and GABACreceptors on BCs were investigated by whole cell recordings and local drug application via multi-barreled puff pipettes in the bullfrog retinal slice preparation. Four types of the BCs (types 1–4) were identified morphologically by injection of Lucifer yellow. According to the ramification levels of the axon terminals and the responses of these cells to glutamate (or kainate) applied at their dendrites, types 1 and 2 of BCs were supposed to be off type, whereas types 3 and 4 of BCs might be on type. Bicuculline (BIC), a GABAA receptor antagonist, and imidazole-4-acetic acid (I4AA), a GABAC receptor antagonist, were used to distinguish GABA receptor-mediated responses. In all BCs tested, not only the axon terminals but also the dendrites showed high GABA sensitivity mediated by both GABAA and GABACreceptors. Subcellular localization and complements of GABAA and GABAC receptors at the dendrites and axon terminals were highly related to the dichotomy of offand on BCs. In the case of off BCs, GABAA receptors were rather evenly distributed at the dendrites and axon terminals, but GABAC receptors were predominantly expressed at the axon terminals. Moreover, the relative contribution of GABAC receptors to the axon terminals was prevalent over that of GABAA receptors, while the situation was reversed at the dendrites. In the case of on BCs, GABAA and GABAC receptors both preferred to be expressed at the axon terminals; relative contributions of these two GABA receptor subtypes to both the sites were comparable, while GABAC receptors were much less expressed than GABAA receptors. GABAA, but not GABAC receptors, were expressed clusteringly at axons of a population of BCs. In a minority of BCs, I4AA suppressed the GABAC responses at the dendrites, but not at the axon terminal, implying that the GABAC receptors at these two sites may be heterogeneous. Taken together, these results suggest that GABAA and GABAC receptors may play different roles in the outer and inner retina and the differential complements of the two receptors on off and on BCs may be closely related to physiological functions of these cells.

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Genetic and Molecular Characterization of the Maizerp3Rust Resistance Locus

Genetics ◽

10.1093/genetics/162.1.381 ◽

2002 ◽

Vol 162 (1) ◽

pp. 381-394 ◽

Cited By ~ 6

Author(s):

Craig A Webb ◽

Todd E Richter ◽

Nicholas C Collins ◽

Marie Nicolas ◽

Harold N Trick ◽

...

Keyword(s):

Family Members ◽

Crossing Over ◽

Resistance Locus ◽

Leucine Rich Repeat ◽

Bac Contig ◽

Puccinia Sorghi ◽

Coding Regions ◽

Complex Locus ◽

Sequence Identities

AbstractIn maize, the Rp3 gene confers resistance to common rust caused by Puccinia sorghi. Flanking marker analysis of rust-susceptible rp3 variants suggested that most of them arose via unequal crossing over, indicating that rp3 is a complex locus like rp1. The PIC13 probe identifies a nucleotide binding site-leucine-rich repeat (NBS-LRR) gene family that maps to the complex. Rp3 variants show losses of PIC13 family members relative to the resistant parents when probed with PIC13, indicating that the Rp3 gene is a member of this family. Gel blots and sequence analysis suggest that at least 9 family members are at the locus in most Rp3-carrying lines and that at least 5 of these are transcribed in the Rp3-A haplotype. The coding regions of 14 family members, isolated from three different Rp3-carrying haplotypes, had DNA sequence identities from 93 to 99%. Partial sequencing of clones of a BAC contig spanning the rp3 locus in the maize inbred line B73 identified five different PIC13 paralogues in a region of ∼140 kb.

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