Membrane topology of the cyanobacterial bicarbonate transporter, BicA, a member of the SulP (SLC26A) family

The cyanobacterial Na+-dependent HCO3– transporter BicA is a member of the ubiquitous and important SulP/SLC26 family of anion transporters found in eukaryotes and prokaryotes. BicA is an important component of the cyanobacterial CO2 concentrating mechanism, an adaptation that contributes to cyanobacteria being able to achieve an estimated 25% of global primary productivity, largely in the oceans. The human SLC26 members are involved in a range of key cellular functions involving a diverse range of anion transport activities including Cl–/HCO3–, I–/HCO3–, and SO42–/HCO3– exchange; mutations in SLC26 members are known to be associated with debilitating diseases such as Pendred syndrome, chondrodysplasias, and congenital chloride diarrhoea. We have recently experimentally determined the membrane topology of BicA using the phoA–lacZ reporter system and here consider some of the extrapolated implications for topology of the human SLC26 family and the Sultr plant sulphate transporters.

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Membrane topology of the cyanobacterial bicarbonate transporter, SbtA, and identification of potential regulatory loops

Molecular Membrane Biology ◽

10.3109/09687688.2011.593049 ◽

2011 ◽

Vol 28 (5) ◽

pp. 265-275 ◽

Cited By ~ 17

Author(s):

G. Dean Price ◽

Megan C. Shelden ◽

Susan M. Howitt

Keyword(s):

Membrane Topology ◽

Bicarbonate Transporter

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Mitochondrial proton/phosphate transporter. An antibody directed against the COOH terminus and proteolytic cleavage experiments provides new insights about its membrane topology.

Journal of Biological Chemistry ◽

10.1016/s0021-9258(17)45346-4 ◽

1990 ◽

Vol 265 (34) ◽

pp. 21202-21206

Author(s):

G C Ferreira ◽

R D Pratt ◽

P L Pedersen

Keyword(s):

Proteolytic Cleavage ◽

Phosphate Transporter ◽

Membrane Topology

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Autosomal recessive congenital hereditary corneal dystrophy associated with a novel SLC4A11 mutation in two consanguineous Tunisian families

British Journal of Ophthalmology ◽

10.1136/bjophthalmol-2020-318204 ◽

2021 ◽

pp. bjophthalmol-2020-318204

Author(s):

Zohra Chibani ◽

Imen Zone Abid ◽

Peter Söderkvist ◽

Jamel Feki ◽

Mounira Hmani Aifa

Keyword(s):

Autosomal Recessive ◽

Corneal Transplantation ◽

Gene Mutations ◽

In Silico Analysis ◽

Corneal Dystrophy ◽

Solute Carrier Family ◽

Transporter Protein ◽

Bicarbonate Transporter ◽

Corneal Clouding ◽

Solute Carrier

BackgroundAutosomal recessive congenital hereditary corneal dystrophy (CHED) is a rare isolated developmental anomaly of the eye characterised by diffuse bilateral corneal clouding that may lead to visual impairment requiring corneal transplantation. CHED is known to be caused by mutations in the solute carrier family 4 member 11 (SLC4A11) gene which encodes a membrane transporter protein (sodium bicarbonate transporter-like solute carrier family 4 member 11).MethodsTo identify SLC4A11 gene mutations associated with CHED (OMIM: #217700), genomic DNA was extracted from whole blood and sequenced for all exons and intron-exon boundaries in two large Tunisian families.ResultsA novel deletion SLC4A11 mutation (p. Leu479del; c.1434_1436del) is responsible for CHED in both analysed families. This non-frameshift mutation was found in a homozygous state in affected members and heterozygous in non-affected members. In silico analysis largely support the pathogenicity of this alteration that may leads to stromal oedema by disrupting the osmolarity balance. Being localised to a region of alpha-helical secondary structure, Leu479 deletion may induce protein-compromising structural rearrangements.ConclusionTo the best of our knowledge, this is the first clinical and genetic study exploring CHED in Tunisia. The present work also expands the list of pathogenic genotypes in SLC4A11 gene and its associated clinical diagnosis giving more insights into genotype–phenotype correlations.

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