Branchiootic syndrome

04/01/2014 - "Sequence analysis of the target gene bos1, which codes for a class III histidine kinase, revealed that the MR phenotype was associated with Q369P and N373S mutations and that the LR phenotype was associated with either a I365S or a I365N mutation. "
05/01/2010 - "In the present study, the complete two-component histidine kinase gene (Bos1) was sequenced for 10 procymidone-resistant and 3 procymidone-sensitive B. "
01/04/2023 - "Based on RNA-sequence analysis, it was found that hybrid histidine kinase, fungal HHKs, such as BOS1, BcHHK2, and BcHHK17, probably involved in the fludioxonil resistance of B. "
10/01/2020 - "We studied the mutants of the sensor histidine kinase Bos1 and of the MAP kinase Sak1. "
01/01/2018 - "Since one or several allelic mutations in the histidine kinase (Bos1) and β-tubulin genes generally confer the resistance to fungicides, the sequences of these target genes were investigated in the selected isolates, which allowed the identification of two different haplotypes. "

10/01/1992 - "In a previous study, we reported that BOS1 encodes a putative 27 kDa membrane protein. "
09/14/2000 - "In yeast, four integral membrane proteins, Sed5, Bos1, Sec22 and Bet1 (refs 2-6), each probably contribute a single helix to form the SNARE complex that is needed for transport from endoplasmic reticulum to Golgi. "
05/21/1993 - "BOS1 encodes an integral endoplasmic reticulum (ER) membrane protein and genetically interacts with three other yeast genes (BET1, SEC22, and YPT1) whose products are required for membrane traffic between the ER and the Golgi apparatus. "
04/01/1991 - "The BOS1 gene encodes an essential 27-kD putative membrane protein that is required for vesicular transport from the ER to the Golgi complex in yeast."
09/30/1994 - "Genetic interactions connect sec27-1 and sec21-1 (coatomer gamma subunit) with the ARF1 and ARF2 genes and with the SEC22, BET1, and BOS1 genes, which encode membrane proteins involved in ER-to-Golgi transport."

05/01/2010 - "In the present study, the complete two-component histidine kinase gene (Bos1) was sequenced for 10 procymidone-resistant and 3 procymidone-sensitive B. "
01/29/2022 - "Moreover, the cell membrane functions of B.cinerea, histidine kinase activity, relative conductivity, triglyceride, and cell membrane structure were determined, and the target gene histidine kinase Bos1 (AF396827.2) of procymidone was amplified and sequenced. "
05/01/2010 - "Isolates representing four different procymidone-resistant phenotypes (CarRDieSPrcRPyrS, CarRDieRPrcRPyrS, CarRDieRPrcRPyrR, and CarRDieRPrcRPyrR) all had nucleic acid point mutations resulting in amino acid changes at position 369 (change from glutamine to proline) as well as at amino acid position 373 (asparagine to serine) in the Bos1 gene."

09/04/2022 - "Our results show that the choice of an array should be based on a balance between the objective of the study and the breed/population considered, with the HD and BOS1 arrays being the best choice for both taurine and indicine breeds when performing GWAS, and the GGPF250 being preferable for fine-mapping studies. "

09/04/2022 - "Our results show that the choice of an array should be based on a balance between the objective of the study and the breed/population considered, with the HD and BOS1 arrays being the best choice for both taurine and indicine breeds when performing GWAS, and the GGPF250 being preferable for fine-mapping studies. "

05/30/2023 - "Using purified proteins, we show that Bos1 and Bet1 bind the Uso1 GHD directly. "
01/01/2023 - "BOS1 protein was mainly localized in the nucleus. "
08/01/2015 - "Pyrosequencing revealed that amino acid substitutions in the target proteins Bos1 (I365S/N, V368F + Q369H), CytB (G143A), Erg27 (F412S), and SdhB (P225F, N230I, and H272R/Y) were associated with reduced sensitivity levels to the corresponding fungicide classes. "
06/14/2010 - "Proteomic analysis of vesicular fractions from the cells aforementioned and additional mutants with defects in conventional secretion pathways (sec1-1, fusion of Golgi-derived exocytic vesicles with the plasma membrane; bos1-1, vesicle targeting to the Golgi complex) or MVB functionality (vps23, late endosomal trafficking) revealed a complex and interrelated protein collection. "
04/03/2000 - "To determine in which membranes protein function is required, temperature-sensitive alleles of BOS1, BET1, SED5, SLY1, and YPT1 that prevent ER/Golgi transport in vitro at restrictive temperatures were used to selectively inactivate these gene products on vesicles or on Golgi membranes. "

04/01/2014 - "These data suggest that, in addition to point mutations in bos1, drug efflux pump activity and potentially a third mechanism of resistance may be contributing to the iprodione HR phenotype. "
01/01/2017 - "The linkage map also identified two mutations, located in the previously described genes Bos1 and BcsdhB, that conferred resistance to the fungicides boscalid and iprodione. "
01/01/2012 - "Functional and structural comparison of pyrrolnitrin- and iprodione-induced modifications in the class III histidine-kinase Bos1 of Botrytis cinerea."
01/01/2017 - "cinerea for carbendazim (E198A mutation in tubA), azoxystrobin (G143A in cytB), iprodione (G367A+V368F in bos1), and MDR1 (gain-of-function mutations in the transcription factor mrr1 gene and overexpression of the drug efflux transporter gene atrB). "
11/01/2016 - "Resistance to boscalid, fenhexamid, iprodione, and pyraclostrobin was found to be caused by amino acid substitutions on target proteins, including H272R/Y in SdhB, F412I/S/V in Erg27, I365 N/S in Bos1, and G143A in Cytb, respectively. "

08/22/2003 - "COPII favors Sed5 within the Sed5/Bos1/Sec22 t-SNARE complex because t-SNARE assembly removes autoinhibitory contacts to expose the YNNSNPF motif. "
04/16/2002 - "Sed5 is known to combine with two light chains (Bos1 and Sec22) to form the t-SNARE needed to receive vesicles from the endoplasmic reticulum. "
01/01/2016 - "We have demonstrated an increase in secretory titers for the Talaromyces emersonii Cel7A (Te-Cel7A, a cellobiohydrolase) and the Saccharomycopsis fibuligera Cel3A (Sf-Cel3A, a β-glucosidase) expressed in Saccharomyces cerevisiae through single and co-overexpression of some of the endoplasmic reticulum (ER)-to-Golgi SNAREs (BOS1, BET1, SEC22 and SED5). "
09/14/2000 - "Fusion only occurs when the v-SNARE Bet1 is on one membrane and the syntaxin heavy chain Sed5 and its two light chains, Bos1 and Sec22, are on the other membrane where they form a functional t-SNARE. "
02/01/1999 - "The glo3Delta and gcs1Delta single mutations each interact with a sec21 mutation that affects a component of COPI, which mediates vesicular transport within the ER-Golgi shuttle, while increased dosage of the BET1, BOS1 and SEC22 genes encoding members of a v-SNARE family that functions within the ER-Golgi alleviates the effects of a glo3Delta mutation. "

08/01/2015 - "The amino acid change I365S, I365N, or V368F + Q369H in Bos1 and H272R in SdhB by itself showed EC50 values of 3.99 to 14.73 ppm, 3.87 to 5.37 ppm, 4.81 to 15.63 ppm, and 2.071 to ≥30 ppm, respectively. "
01/01/2023 - "The bos1-1 mutation was located in chromosome 1. A T-to-A mutation in BOS1 was identified, which changed the codon from TAC to AAC, resulting in the amino acid change from tyrosine to asparagine. "
11/01/2018 - "A total of three rare missense mutations were detected, including heterozygous c.244G>A in LMNA, c.546C>G in potassium voltage‑gated channel subfamily KQT (KCNQ4) and c.1276G>A in EYA transcriptional coactivator and phosphatase 1 (EYA1), indicating a glutamic acid to lysine substitution at amino acid 82 (p.E82K) in LMNA, a p.F182L in KCNQ4 (a mutation associated with pathogenic deafness) and p.G426S in EYA1 (associated with Branchiootorenal syndrome 1 and Branchiootic syndrome 1 pathogenesis). "
04/01/2020 - "Sequence analysis of their BOs1 sequences indicated that the fludioxonil-resistant field isolate, XXtom1806, had four point mutations resulting in four amino acid changes (I365S, S531G, T565N, and T1267A) and three amino acids (I365S, S531G, and T565N) in the histidine kinases, adenylyl cyclases, methyl-accepting chemotaxis receptors, and phosphatases domain, which associated with fludioxonil binding. "
05/01/2010 - "Isolates representing four different procymidone-resistant phenotypes (CarRDieSPrcRPyrS, CarRDieRPrcRPyrS, CarRDieRPrcRPyrR, and CarRDieRPrcRPyrR) all had nucleic acid point mutations resulting in amino acid changes at position 369 (change from glutamine to proline) as well as at amino acid position 373 (asparagine to serine) in the Bos1 gene."

09/01/2018 - "Molecular analyses of the cytochrome b, β-tubulin, and bos1 genes revealed the presence of G143A; E198A; and I365 N/S, Q369P, or N373S mutations, respectively, in resistant isolates of B. "
01/01/2018 - "Since one or several allelic mutations in the histidine kinase (Bos1) and β-tubulin genes generally confer the resistance to fungicides, the sequences of these target genes were investigated in the selected isolates, which allowed the identification of two different haplotypes. "
03/09/2021 - "Resistance conferring mutations were found in a selection of isolates characterized as resistant to thiophanate-methyl, iprodione, pyraclostrobin, fenhexamid, and boscalid including E198A in β-tubulin; I365N/S, Q369P, and N373S in bos1; G143A in cytb; P238S, N369D, and F412I/S in erg27; and P225F and H272R/Y in sdhB, respectively. "
04/01/2015 - "Resistance to thiophanate-methyl, iprodione, boscalid, pyraclostrobin, and fenhexamid was based on target gene mutations that conferred E198A and F200Y in β-tubulin, I365N/S in Bos1, H272R/Y in SdhB, G143A in Cytb, and T63I and F412S in Erg27. "