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Splice-variant 1 of the ancient domain protein 2 (ACDP2) complements the magnesium-deficient growth phenotype of Salmonella enterica sv. typhimurium strain MM281


Magnesium Research. Volume 23, Number 2, 105-14, June 2010, original article

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Author(s) : Gerhard Sponder, Sona Svidova, Monika Schweigel, Jürgen Vormann, Martin Kolisek

Summary : Evidence arguing for the existence of genes encoding for proteins directly involved in the transport of Mg 2+ through the cytoplasmic membrane have accumulated over the last few years. Gene ACDP2 (ancient conserved domain protein 2\; old name CNNM2, cyclin M2) is one such gene. ACDP2 is a distant homologue of the bacterial gene corC, which is known to be involved in cobalt resistance. We have previously demonstrated that the over-expression of the human Mg 2+ carrier SLC41A1 partly complements the Mg 2+-dependent growth deficiency of Salmonella strain MM281 (triple disruptant in genes: mgtA, mgtB and corA) cultivated in media containing growth non-permissive [Mg 2+] e. We have used the same approach to examine whether over-expressed human ACDP2 has a similar efficacy to complement growth deficiency of the MM281 strain in media containing growth non-permissive [Mg 2+] e. Two splicing variants of the ACDP2 gene have been tested. Here, we show that over-expressed isomorph 1 is efficient in restoring growth of the MM281 strain in media containing growth non-permissive [Mg 2+] e, whereas isomorph 2 is not. Therefore, we conclude that ACDP2sp.v.1 is a functional Mg 2+-transporting entity per se. Our conclusion is supported by the measurable Mg 2+ influx seen in MM281 bacteria over-expressing ACDP2sp.v.1 but not in MM281 bacteria over-expressing ACDP2sp.v.2 or in cells transformed with the empty vector.

Keywords : ACDP2, genetic complementation, Salmonella sp., magnesium transporter, mag-fura 2

 

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