What question did this study set out to answer?

To investigate the functional and regulatory relationship between TMEM165 and the Golgi calcium/manganese pump SPCA1.

October 17, 2019Biochemical Journal

Investigating the functional link between TMEM165 and SPCA1

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Authors

ELElodie Lebredonchel MHMarine Houdou HHHans-Heinrich Hoffmann

Discussion

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Overview

In vitro study reveals that SPCA1 manganese pumping prevents lysosomal degradation of TMEM165 in Hap1 cells, indicating a coordinated mechanism for maintaining Golgi ion balance.

Key Points

To investigate the functional and regulatory relationship between TMEM165 and the Golgi calcium/manganese pump SPCA1.
Assessed TMEM165 stability and lysosomal degradation in SPCA1-deficient Hap1 knockout cells.
Performed rescue assays using wild-type SPCA1, ion-selective SPCA1 mutants (such as the manganese-favoring Q747A mutant), and SERCA2b overexpression.
Deficiency of SPCA1 led to a nearly complete loss of TMEM165 due to constitutive degradation within lysosomes.
TMEM165 expression and Golgi localization were specifically rescued by SPCA1 mutants capable of manganese transport, notably the Q747A mutant.
Overexpression of SERCA2b restored TMEM165 abundance, demonstrating that TMEM165 stability is directly coupled to active intracellular ion pumping.

Cite This Study

Lebredonchel et al. (2019) studied this question.

synapsesocial.com/papers/6aa54edf4bcbe4818eeeb317 https://doi.org/10.1042/bcj20190488

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October 17, 2019Biochemical Journal

Investigating the functional link between TMEM165 and SPCA1

View Full Paper

Ask AI

Bookmark

Authors

ELElodie Lebredonchel MHMarine Houdou HHHans-Heinrich Hoffmann

Discussion

Member takes

Overview

In vitro study reveals that SPCA1 manganese pumping prevents lysosomal degradation of TMEM165 in Hap1 cells, indicating a coordinated mechanism for maintaining Golgi ion balance.

Key Points

To investigate the functional and regulatory relationship between TMEM165 and the Golgi calcium/manganese pump SPCA1.
Assessed TMEM165 stability and lysosomal degradation in SPCA1-deficient Hap1 knockout cells.
Performed rescue assays using wild-type SPCA1, ion-selective SPCA1 mutants (such as the manganese-favoring Q747A mutant), and SERCA2b overexpression.
Deficiency of SPCA1 led to a nearly complete loss of TMEM165 due to constitutive degradation within lysosomes.
TMEM165 expression and Golgi localization were specifically rescued by SPCA1 mutants capable of manganese transport, notably the Q747A mutant.
Overexpression of SERCA2b restored TMEM165 abundance, demonstrating that TMEM165 stability is directly coupled to active intracellular ion pumping.

Cite This Study

Lebredonchel et al. (2019) studied this question.

synapsesocial.com/papers/6aa54edf4bcbe4818eeeb317 https://doi.org/10.1042/bcj20190488

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