The Experts below are selected from a list of 25731 Experts worldwide ranked by ideXlab platform
Minxin Guan - One of the best experts on this subject based on the ideXlab platform.
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biochemical characterization of the deafness associated mitochondrial trnaser ucn a7445g mutation in osteosarcoma cell cybrids
Biochemical and Biophysical Research Communications, 2005Co-Authors: Linda S Zhang, Nathan Fischelghodsian, Minxin GuanAbstract:Abstract The deafness-associated A7445G mutation in the precursor of mitochondrial tRNA Ser(UCN) has been identified in several pedigrees from different ethnic backgrounds. To determine the role of nuclear background in the biochemical manifestation associated with the A7445G mutation, we performed a biochemical characterization of this mutation using cybrids constructed by transferring mitochondria from lymphoblastoid cell lines derived from a New Zealand family into human osteosarcoma mtDNA-less ( ρ 0 ) cells. Compared with three control cybrids, three cybrids derived from an affected matrilineal relative carrying the homoplasmic A7445G mutation exhibited ∼38–57% decrease in the steady-state level of tRNA Ser(UCN) , which is less reduced levels than in lymphoblastoid cells in the previous study. Furthermore, ∼22% reduction in the level of aminoacylation of tRNA Ser(UCN) was observed in the mutant cybrid cells. Interestingly, ∼60–63% decrease of steady-state level of ND6 gene, which belongs to the same precursor as that of tRNA Ser(UCN) , in cybrid cell lines carrying the A7445G mutation, is more than that observed in lymphoblastoid cells. These observations strongly point out a mechanistic link between the Processing Defect of the tRNA Ser(UCN) precursor and decreased stability of ND6 mRNA precursor. These results also imply the influence of nuclear background on the biochemical phenotype associated with the A7445G mutation.
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the deafness associated mitochondrial dna mutation at position 7445 which affects trnaser ucn precursor Processing has long range effects on nadh dehydrogenase subunit nd6 gene expression
Molecular and Cellular Biology, 1998Co-Authors: Minxin Guan, Nathan Fischelghodsian, Jose Antonio Enriquez, Ram S Puranam, Catherine P Lin, Marion A Maw, Giuseppe AttardiAbstract:The pathogenetic mechanism of the deafness-associated mitochondrial DNA (mtDNA) T7445C mutation has been investigated in several lymphoblastoid cell lines from members of a New Zealand pedigree exhibiting the mutation in homoplasmic form and from control individuals. We show here that the mutation flanks the 3' end of the tRNASer(UCN) gene sequence and affects the rate but not the sites of Processing of the tRNA precursor. This causes an average reduction of ~70% in the tRNASer(UCN) level and a decrease of ~45% in protein synthesis rate in the cell lines analyzed. The data show a sharp threshold in the capacity of tRNASer(UCN) to support the wild-type protein synthesis rate, which corresponds to ~40% of the control level of this tRNA. Strikingly, a 7445 mutation-associated marked reduction has been observed in the level of the mRNA for the NADH dehydrogenase (complex I) ND6 subunit gene, which is located ~7 kbp upstream and is cotranscribed with the tRNASer(UCN) gene, with strong evidence pointing to a mechanistic link with the tRNA precursor Processing Defect. Such reduction significantly affects the rate of synthesis of the ND6 subunit and plays a determinant role in the deafness-associated respiratory phenotype of the mutant cell lines. In particular, it accounts for their specific, very significant decrease in glutamate- or malate-dependent O2 consumption. Furthermore, several homoplasmic mtDNA mutations affecting subunits of NADH dehydrogenase may play a synergistic role in the establishment of the respiratory phenotype of the mutant cells.
Graham C Walker - One of the best experts on this subject based on the ideXlab platform.
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sinorhizobium meliloti ybey is a zinc dependent single strand specific endoribonuclease that plays an important role in 16s ribosomal rna Processing
Nucleic Acids Research, 2020Co-Authors: Vignesh M P Babu, Siva Sankari, James A Budnick, Clayton C Caswell, Graham C WalkerAbstract:: Single-strand specific endoribonuclease YbeY has been shown to play an important role in the Processing of the 3' end of the 16S rRNA in Escherichia coli. Lack of YbeY results in the accumulation of the 17S rRNA precursor. In contrast to a previous report, we show that Sinorhizobium meliloti YbeY exhibits endoribonuclease activity on single-stranded RNA substrate but not on the double-stranded substrate. This study also identifies the previously unknown metal ion involved in YbeY function to be Zn2+ and shows that the activity of YbeY is enhanced when the occupancy of zinc is increased. We have identified a pre-16S rRNA precursor that accumulates in the S. meliloti ΔybeY strain. We also show that ΔybeY mutant of Brucella abortus, a mammalian pathogen, also accumulates a similar pre-16S rRNA. The pre-16S species is longer in alpha-proteobacteria than in gamma-proteobacteria. We demonstrate that the YbeY from E. coli and S. meliloti can reciprocally complement the rRNA Processing Defect in a ΔybeY mutant of the other organism. These results establish YbeY as a zinc-dependent single-strand specific endoribonuclease that functions in 16S rRNA Processing in both alpha- and gamma-proteobacteria.
James A Budnick - One of the best experts on this subject based on the ideXlab platform.
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sinorhizobium meliloti ybey is a zinc dependent single strand specific endoribonuclease that plays an important role in 16s ribosomal rna Processing
Nucleic Acids Research, 2020Co-Authors: Vignesh M P Babu, Siva Sankari, James A Budnick, Clayton C Caswell, Graham C WalkerAbstract:: Single-strand specific endoribonuclease YbeY has been shown to play an important role in the Processing of the 3' end of the 16S rRNA in Escherichia coli. Lack of YbeY results in the accumulation of the 17S rRNA precursor. In contrast to a previous report, we show that Sinorhizobium meliloti YbeY exhibits endoribonuclease activity on single-stranded RNA substrate but not on the double-stranded substrate. This study also identifies the previously unknown metal ion involved in YbeY function to be Zn2+ and shows that the activity of YbeY is enhanced when the occupancy of zinc is increased. We have identified a pre-16S rRNA precursor that accumulates in the S. meliloti ΔybeY strain. We also show that ΔybeY mutant of Brucella abortus, a mammalian pathogen, also accumulates a similar pre-16S rRNA. The pre-16S species is longer in alpha-proteobacteria than in gamma-proteobacteria. We demonstrate that the YbeY from E. coli and S. meliloti can reciprocally complement the rRNA Processing Defect in a ΔybeY mutant of the other organism. These results establish YbeY as a zinc-dependent single-strand specific endoribonuclease that functions in 16S rRNA Processing in both alpha- and gamma-proteobacteria.
Giuseppe Attardi - One of the best experts on this subject based on the ideXlab platform.
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the deafness associated mitochondrial dna mutation at position 7445 which affects trnaser ucn precursor Processing has long range effects on nadh dehydrogenase subunit nd6 gene expression
Molecular and Cellular Biology, 1998Co-Authors: Minxin Guan, Nathan Fischelghodsian, Jose Antonio Enriquez, Ram S Puranam, Catherine P Lin, Marion A Maw, Giuseppe AttardiAbstract:The pathogenetic mechanism of the deafness-associated mitochondrial DNA (mtDNA) T7445C mutation has been investigated in several lymphoblastoid cell lines from members of a New Zealand pedigree exhibiting the mutation in homoplasmic form and from control individuals. We show here that the mutation flanks the 3' end of the tRNASer(UCN) gene sequence and affects the rate but not the sites of Processing of the tRNA precursor. This causes an average reduction of ~70% in the tRNASer(UCN) level and a decrease of ~45% in protein synthesis rate in the cell lines analyzed. The data show a sharp threshold in the capacity of tRNASer(UCN) to support the wild-type protein synthesis rate, which corresponds to ~40% of the control level of this tRNA. Strikingly, a 7445 mutation-associated marked reduction has been observed in the level of the mRNA for the NADH dehydrogenase (complex I) ND6 subunit gene, which is located ~7 kbp upstream and is cotranscribed with the tRNASer(UCN) gene, with strong evidence pointing to a mechanistic link with the tRNA precursor Processing Defect. Such reduction significantly affects the rate of synthesis of the ND6 subunit and plays a determinant role in the deafness-associated respiratory phenotype of the mutant cell lines. In particular, it accounts for their specific, very significant decrease in glutamate- or malate-dependent O2 consumption. Furthermore, several homoplasmic mtDNA mutations affecting subunits of NADH dehydrogenase may play a synergistic role in the establishment of the respiratory phenotype of the mutant cells.
Nathan Fischelghodsian - One of the best experts on this subject based on the ideXlab platform.
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biochemical characterization of the deafness associated mitochondrial trnaser ucn a7445g mutation in osteosarcoma cell cybrids
Biochemical and Biophysical Research Communications, 2005Co-Authors: Linda S Zhang, Nathan Fischelghodsian, Minxin GuanAbstract:Abstract The deafness-associated A7445G mutation in the precursor of mitochondrial tRNA Ser(UCN) has been identified in several pedigrees from different ethnic backgrounds. To determine the role of nuclear background in the biochemical manifestation associated with the A7445G mutation, we performed a biochemical characterization of this mutation using cybrids constructed by transferring mitochondria from lymphoblastoid cell lines derived from a New Zealand family into human osteosarcoma mtDNA-less ( ρ 0 ) cells. Compared with three control cybrids, three cybrids derived from an affected matrilineal relative carrying the homoplasmic A7445G mutation exhibited ∼38–57% decrease in the steady-state level of tRNA Ser(UCN) , which is less reduced levels than in lymphoblastoid cells in the previous study. Furthermore, ∼22% reduction in the level of aminoacylation of tRNA Ser(UCN) was observed in the mutant cybrid cells. Interestingly, ∼60–63% decrease of steady-state level of ND6 gene, which belongs to the same precursor as that of tRNA Ser(UCN) , in cybrid cell lines carrying the A7445G mutation, is more than that observed in lymphoblastoid cells. These observations strongly point out a mechanistic link between the Processing Defect of the tRNA Ser(UCN) precursor and decreased stability of ND6 mRNA precursor. These results also imply the influence of nuclear background on the biochemical phenotype associated with the A7445G mutation.
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the deafness associated mitochondrial dna mutation at position 7445 which affects trnaser ucn precursor Processing has long range effects on nadh dehydrogenase subunit nd6 gene expression
Molecular and Cellular Biology, 1998Co-Authors: Minxin Guan, Nathan Fischelghodsian, Jose Antonio Enriquez, Ram S Puranam, Catherine P Lin, Marion A Maw, Giuseppe AttardiAbstract:The pathogenetic mechanism of the deafness-associated mitochondrial DNA (mtDNA) T7445C mutation has been investigated in several lymphoblastoid cell lines from members of a New Zealand pedigree exhibiting the mutation in homoplasmic form and from control individuals. We show here that the mutation flanks the 3' end of the tRNASer(UCN) gene sequence and affects the rate but not the sites of Processing of the tRNA precursor. This causes an average reduction of ~70% in the tRNASer(UCN) level and a decrease of ~45% in protein synthesis rate in the cell lines analyzed. The data show a sharp threshold in the capacity of tRNASer(UCN) to support the wild-type protein synthesis rate, which corresponds to ~40% of the control level of this tRNA. Strikingly, a 7445 mutation-associated marked reduction has been observed in the level of the mRNA for the NADH dehydrogenase (complex I) ND6 subunit gene, which is located ~7 kbp upstream and is cotranscribed with the tRNASer(UCN) gene, with strong evidence pointing to a mechanistic link with the tRNA precursor Processing Defect. Such reduction significantly affects the rate of synthesis of the ND6 subunit and plays a determinant role in the deafness-associated respiratory phenotype of the mutant cell lines. In particular, it accounts for their specific, very significant decrease in glutamate- or malate-dependent O2 consumption. Furthermore, several homoplasmic mtDNA mutations affecting subunits of NADH dehydrogenase may play a synergistic role in the establishment of the respiratory phenotype of the mutant cells.