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Background  Chromosome counting is a process in which cells determine somehow their intrinsic chromosome number(s). The best-studied cellular mechanism that involves chromosome counting is ‘chromosome-kissing’ and X-chromosome inactivation (XCI) mechanism. It is necessary for the well-known dosage compensation between the genders in mammals to balance the number of active X-chromosomes (Xa) with regard to diploid set of autosomes. At the onset of XCI, two X-chromosomes are coming in close proximity and pair physically by a specific segment denominated X-pairing region (Xpr) that involves the  SLC16A2  gene.    Results  An Ensembl BLAST search for human and mouse  SLC16A2 / Slc16a2  homologues revealed, that highly similar sequences can be found at almost each chromosome in the corresponding genomes. Additionally, a BLAST search for  SLC16A2 / TSIX / XIST  (genes responsible for XCI) reveled that “ SLC16A2 / TSIX / XIST  like sequences” cover equally all chromosomes, too. With respect to this we provide following hypotheses.    Hypotheses  If a single genomic region containing the  SLC16A2  gene on X-chromosome is responsible for maintaining “balanced” active copy numbers, it is possible that similar sequences or gene/s have the same function on other chromosomes (autosomes).  SLC16A2  like sequences on autosomes could encompass evolutionary older, but functionally active key regions for chromosome counting in early embryogenesis. Also  SLC16A2  like sequence on autosomes could be involved in inappropriate chromosomes pairing and, thereby be involved in aneuploidy formation during embryogenesis and cancer development. Also, “ SLC16A2/TSIX/XIST  gene like sequence combinations” covering the whole genome, could be important for the determination of X:autosome ratio in cells and chromosome counting.    Conclusions   SLC16A2  and/or  SLC16A2/TSIX/XIST  like sequence dispersed across autosomes and X-chromosome(s) could serve as bases for a counting mechanism to determine X:autosome ratio and could potentially be a mechanism by which a cell also counts its autosomes. It could also be that such specific genomic regions have the same function for each specific autosome. As errors during the obviously existing process of chromosome counting are one if not the major origin of germline/somatic aneuploidy the here presented hypotheses should further elaborated and experimentally tested.    Electronic supplementary material  The online version of this article (doi:10.1186/s13039-016-0271-7) contains supplementary material, which is available to authorized users.

Thoughts about SLC16A2, TSIX and XIST gene like sites in the human genome and a potential role in cellular chromosome counting