Title : Lack of plasma membrane targeting of a G172D mutant thiamine transporter derived from Rogers syndrome family
Abstract :
- BACKGROUND: Rogers syndrome, also known as thiamine responsive megaloblastic anemia ( TRMA ), is an autosomal recessive disorder resulting in megaloblastic anemia, diabetes mellitus and sensorineural deafness
- The gene associated with Rogers syndrome encodes for a plasma membrane thiamine transporter, THTR-1 , a member of the solute carrier family that includes its homologue THTR-2 and the reduced folate carrier
- MATERIALS AND METHODS: Using transient expression of wild-type and a missense mutant THTR-1 protein , derived from a TRMA family, in different cell lines and immunodetection analysis, we determined the expression, posttranslational modification, and subcellular localization of the wild-type and G172D mutant THTR-1
- The transport activity of the transfected THTR-1 proteins was measured using a [(3) H ] thiamine uptake assay
- RESULTS: The mutant THTR-1 protein was undetectable in transfected cells grown at 37 degrees C but was readily expressed in transfected cells cultured at 28 degrees C, thereby allowing for further biochemical and functional analysis
- In contrast to its fully glycosylated wild-type mature protein , the mutant THTR-1 protein underwent only the initial stage of N-linked glycosylation
- The failure to undergo a complete glycosylation resulted in the lack of plasma membrane targeting and confinement of the mutant THTR-1 to the Golgi and endoplasmic reticulum (ER) compartment
- Consistently, either treatment with tunicamycin or substitution of the THTR-1 consensus N-glycosylation acceptor asparagine 63 with glutamine , abolished its glycosylation and plasma membrane targeting
- CONCLUSIONS: Taken collectively, these results suggest that the G172D mutation presumably misfolded THTR-1 protein that fails to undergo a complete glycosylation, is retained in the Golgi-ER compartment and thereby cannot be targeted to the plasma membrane
- Finally, transfection studies revealed that the mutant G172D THTR-1 failed to transport thiamine
- This is the first molecular and functional characterization of a missense mutant THTR-1 derived from a family with Rogers syndrome
Output (sent_index, trigger,
protein,
sugar,
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- 6. glycosylated, , protein, -, -
- 9. glycosylation, , THTR-1 protein, -, -
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protein,
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*Output_Site_Fusion* (sent_index,
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