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John E. Donelson - One of the best experts on this subject based on the ideXlab platform.
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Inhibition of Protein Phosphatase 1 and 2A Down-Regulates β-Tubulin Gene Expression in Trypanosoma Rhodesiense
Biochemical and biophysical research communications, 1995Co-Authors: John E. DonelsonAbstract:Abstract We studied the effect of okadaic acid, a specific inhibitor of serine/threonine protein phosphatase types 1 and 2A, on the expression of β-tubulin and procyclin genes in Trypanosoma Rhodesiense . Okadaic acid was found to decrease the steady-state level of β-tubulin mRNA about 5-fold in differentiating bloodstream trypanosomes and about 3-fold in established procyclic trypanosomes. No effect was observed on the expression of the procyclin gene. The down-regulation of β-tubulin gene expression by okadaic acid in procyclic trypanosomes occurs at the post-transcriptional level. These results demonstrate the involvement of protein phosphatase 1 and/or 2A activity in maintaining the steady-state level of β-tubulin mRNA in African trypanosomes.
Etienne Pays - One of the best experts on this subject based on the ideXlab platform.
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Adaptation of Trypanosoma Rhodesiense to hypohaptoglobinaemic serum requires transcription of the APOL1 resistance gene in a RNA polymerase I locus.
Molecular microbiology, 2015Co-Authors: Laurence Lecordier, Pierrick Uzureau, Patricia Tebabi, Jonathan Brauner, Fleur Samantha Benghiat, Benoit Vanhollebeke, Etienne PaysAbstract:Human apolipoprotein L1 (APOL1) kills African trypanosomes except Trypanosoma Rhodesiense and Trypanosoma gambiense, the parasites causing sleeping sickness. APOL1 uptake into trypanosomes is favoured by its association with the haptoglobin-related protein-haemoglobin complex, which binds to the parasite surface receptor for haptoglobin-haemoglobin. As haptoglobin-haemoglobin can saturate the receptor, APOL1 uptake is increased in haptoglobin-poor (hypohaptoglobinaemic) serum (HyHS). While T. Rhodesiense resists APOL1 by RNA polymerase I (pol-I)-mediated expression of the serum resistance-associated (SRA) protein, T. gambiense resists by pol-II-mediated expression of the T. gambiense-specific glycoprotein (TgsGP). Moreover, in T. gambiense resistance to HyHS is linked to haptoglobin-haemoglobin receptor inactivation by mutation. We report that unlike T. gambiense, T. Rhodesiense possesses a functional haptoglobin-haemoglobin receptor, and that like T. gambiense experimentally provided with active receptor, this parasite is killed in HyHS because of receptor-mediated APOL1 uptake. However, T. Rhodesiense could adapt to low haptoglobin by increasing transcription of SRA. When assayed in Trypanosoma brucei, resistance to HyHS occurred with pol-I-, but not with pol-II-mediated SRA expression. Similarly, T. gambiense provided with active receptor acquired resistance to HyHS only when TgsGP was moved to a pol-I locus. Thus, transcription by pol-I favours adaptive gene regulation, explaining the presence of SRA in a pol-I locus.
Laurence Lecordier - One of the best experts on this subject based on the ideXlab platform.
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Adaptation of Trypanosoma Rhodesiense to hypohaptoglobinaemic serum requires transcription of the APOL1 resistance gene in a RNA polymerase I locus.
Molecular microbiology, 2015Co-Authors: Laurence Lecordier, Pierrick Uzureau, Patricia Tebabi, Jonathan Brauner, Fleur Samantha Benghiat, Benoit Vanhollebeke, Etienne PaysAbstract:Human apolipoprotein L1 (APOL1) kills African trypanosomes except Trypanosoma Rhodesiense and Trypanosoma gambiense, the parasites causing sleeping sickness. APOL1 uptake into trypanosomes is favoured by its association with the haptoglobin-related protein-haemoglobin complex, which binds to the parasite surface receptor for haptoglobin-haemoglobin. As haptoglobin-haemoglobin can saturate the receptor, APOL1 uptake is increased in haptoglobin-poor (hypohaptoglobinaemic) serum (HyHS). While T. Rhodesiense resists APOL1 by RNA polymerase I (pol-I)-mediated expression of the serum resistance-associated (SRA) protein, T. gambiense resists by pol-II-mediated expression of the T. gambiense-specific glycoprotein (TgsGP). Moreover, in T. gambiense resistance to HyHS is linked to haptoglobin-haemoglobin receptor inactivation by mutation. We report that unlike T. gambiense, T. Rhodesiense possesses a functional haptoglobin-haemoglobin receptor, and that like T. gambiense experimentally provided with active receptor, this parasite is killed in HyHS because of receptor-mediated APOL1 uptake. However, T. Rhodesiense could adapt to low haptoglobin by increasing transcription of SRA. When assayed in Trypanosoma brucei, resistance to HyHS occurred with pol-I-, but not with pol-II-mediated SRA expression. Similarly, T. gambiense provided with active receptor acquired resistance to HyHS only when TgsGP was moved to a pol-I locus. Thus, transcription by pol-I favours adaptive gene regulation, explaining the presence of SRA in a pol-I locus.
Pierrick Uzureau - One of the best experts on this subject based on the ideXlab platform.
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Adaptation of Trypanosoma Rhodesiense to hypohaptoglobinaemic serum requires transcription of the APOL1 resistance gene in a RNA polymerase I locus.
Molecular microbiology, 2015Co-Authors: Laurence Lecordier, Pierrick Uzureau, Patricia Tebabi, Jonathan Brauner, Fleur Samantha Benghiat, Benoit Vanhollebeke, Etienne PaysAbstract:Human apolipoprotein L1 (APOL1) kills African trypanosomes except Trypanosoma Rhodesiense and Trypanosoma gambiense, the parasites causing sleeping sickness. APOL1 uptake into trypanosomes is favoured by its association with the haptoglobin-related protein-haemoglobin complex, which binds to the parasite surface receptor for haptoglobin-haemoglobin. As haptoglobin-haemoglobin can saturate the receptor, APOL1 uptake is increased in haptoglobin-poor (hypohaptoglobinaemic) serum (HyHS). While T. Rhodesiense resists APOL1 by RNA polymerase I (pol-I)-mediated expression of the serum resistance-associated (SRA) protein, T. gambiense resists by pol-II-mediated expression of the T. gambiense-specific glycoprotein (TgsGP). Moreover, in T. gambiense resistance to HyHS is linked to haptoglobin-haemoglobin receptor inactivation by mutation. We report that unlike T. gambiense, T. Rhodesiense possesses a functional haptoglobin-haemoglobin receptor, and that like T. gambiense experimentally provided with active receptor, this parasite is killed in HyHS because of receptor-mediated APOL1 uptake. However, T. Rhodesiense could adapt to low haptoglobin by increasing transcription of SRA. When assayed in Trypanosoma brucei, resistance to HyHS occurred with pol-I-, but not with pol-II-mediated SRA expression. Similarly, T. gambiense provided with active receptor acquired resistance to HyHS only when TgsGP was moved to a pol-I locus. Thus, transcription by pol-I favours adaptive gene regulation, explaining the presence of SRA in a pol-I locus.
Patricia Tebabi - One of the best experts on this subject based on the ideXlab platform.
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Adaptation of Trypanosoma Rhodesiense to hypohaptoglobinaemic serum requires transcription of the APOL1 resistance gene in a RNA polymerase I locus.
Molecular microbiology, 2015Co-Authors: Laurence Lecordier, Pierrick Uzureau, Patricia Tebabi, Jonathan Brauner, Fleur Samantha Benghiat, Benoit Vanhollebeke, Etienne PaysAbstract:Human apolipoprotein L1 (APOL1) kills African trypanosomes except Trypanosoma Rhodesiense and Trypanosoma gambiense, the parasites causing sleeping sickness. APOL1 uptake into trypanosomes is favoured by its association with the haptoglobin-related protein-haemoglobin complex, which binds to the parasite surface receptor for haptoglobin-haemoglobin. As haptoglobin-haemoglobin can saturate the receptor, APOL1 uptake is increased in haptoglobin-poor (hypohaptoglobinaemic) serum (HyHS). While T. Rhodesiense resists APOL1 by RNA polymerase I (pol-I)-mediated expression of the serum resistance-associated (SRA) protein, T. gambiense resists by pol-II-mediated expression of the T. gambiense-specific glycoprotein (TgsGP). Moreover, in T. gambiense resistance to HyHS is linked to haptoglobin-haemoglobin receptor inactivation by mutation. We report that unlike T. gambiense, T. Rhodesiense possesses a functional haptoglobin-haemoglobin receptor, and that like T. gambiense experimentally provided with active receptor, this parasite is killed in HyHS because of receptor-mediated APOL1 uptake. However, T. Rhodesiense could adapt to low haptoglobin by increasing transcription of SRA. When assayed in Trypanosoma brucei, resistance to HyHS occurred with pol-I-, but not with pol-II-mediated SRA expression. Similarly, T. gambiense provided with active receptor acquired resistance to HyHS only when TgsGP was moved to a pol-I locus. Thus, transcription by pol-I favours adaptive gene regulation, explaining the presence of SRA in a pol-I locus.
