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Expression Analysis of the Mouse Multi-Copy X-Linked Gene Xlr-Related, Meiosis-Regulated (Xmr), Reveals That Xmr Encodes a Spermatid-Expressed Cytoplasmic Protein, SLX/XMR¹

MRC National Institute for Medical Research,³ London NW7 1AA, United Kingdom Département Génétique & Développement,⁴ Institut Cochin, Paris F-75014, France Karolinska Institute,⁵ Stockholm, Sweden SE-17177

ABSTRACT

The mouse multi-copy X-linked gene Xlr-related, meiosis-regulated (Xmr/Slx) has previously been described as encoding a testis-specific nuclear protein expressed during male meiotic prophase, and during which it becomes concentrated in the inactive X and Y chromatin domain. These conclusions were based on Western blot and immunolocalization analysis using an antibody raised against a related lymphocyte protein, XLR; however, our recently published RNA in situ for Xmr revealed that transcripts are predominantly or exclusively postmeiotic, and this is supported by a growing body of microarray data. This led us to reanalyze the expression of Xmr, both at the RNA level by RT-PCR and by RNA fluorescence in situ hybridization, and at the protein level by using antibodies raised against XMR that do not recognize XLR. In agreement with our previous RNA in situ data, our further transcription analysis showed almost exclusive expression in spermatids, and Western blot and immunostaining with the XMR antibodies showed that the protein is cytoplasmic and restricted to spermatids. Furthermore, the previously used XLR antibody was shown not to cross-react with XMR, and it is suggested that the meiotically expressed nuclear protein recognized by this antibody is another member of the complex Xlr superfamily. As a result of these findings, the gene previously known as Xmr is now officially know as Slx, Sycp3-like, X-linked.

Cor1 domain,, gametogenesis,, meiosis,, spermatid,, spermatid-specific,, spermatogenesis,, testis,, XLR,, Xlr superfamily,, XMR

¹Supported by an MRC research studentship to L.N.R, a Marie Curie Fellowship to A.T., an EMBO Fellowship to J.C., and a grant from the Swedish Research Council to C.H.

Correspondence: ²FAX: 44 20 8816 2009; pburgoy{at}nimr.mrc.ac.uk

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