aneuploidy or polyploidy. genes on the affected chromosome may be upregulated or down-regulated to compensate for the change in the normal number of chromosomes present. reptiles research into dosage compensation has been carried out in six species of toxicoferan reptiles and in one species of softshell turtle. two species of caenophidian snake (one which belongs to the family viperidae and the other to the family colubridae) have been investigated and both of these exhibit female heterogametic sex determination systems (zz\zw) and have incomplete compensation without balance. the komodo dragon exhibits incomplete compensation without dosage balance in their independently evolved zz/zw system. in the xx/xy system of basiliscus vittatus and multiple neo-sex chromosomes with male heterogamety in the pygopodid gecko lialis burtonis incomplete compensation without dosage balance were also seen. the green anole (anolis carolinensis; dactyloidea), has xx/xy sex determination and unlike the other squamates studied to date has complete dosage compensation with dosage balance. in the florida softshell turtle (apalone ferox) with zz/zw sex chromosomes, the lack of dosage balance in the expression of z-linked genes was also found. x chromosome inactivation and embryonic stem cells xci is initiated very early during female embryonic development or upon differentiation of female embryonic stem (es) cells and results in inactivation of one x chromosome in every female somatic cell. this process is initiated very early during development, around the two- to eight-cell stage and is maintained in the developing extra-embryonic tissues of the embryo, including the fetal placenta. xist rna induces heterochromatinization of the x chromosome by attracting chromatin modifiers, involved in gene silencing. xist rna is tightly associated with the xi and it is required for x chromosome inactivation to occur in cis. knockout studies in female es cells and mice have shown that x chromosomes bearing a deletion of the xist gene are unable to inactivate the mutated x. most of the human female es cell lines display an inactivated x chromosome already in the undifferentiated state characterized by xist expression, xist coating and accumulated markers of heterochromatin on the xi. it is widely thought that human embryos do not employ xci prior to implantation. female embryos have an accumulation of xist rna on one of the two x chromosomes, beginning around the 8-cell stage. xist rna accumulates at the morula and blastocyst stages and is shown to be associated with transcriptional silencing of the xist-coated chromosomal region, therefore indicating dosage compensation has occurred. recently, however, it has become increasingly apparent that xci of the paternal x chromosome is already present from the 4-cell stage onward in all cells of preimplantation mouse embryos, not the 8-cell stages. xist, xite, and tsix and their roles in x-inactivation xite and xist, are both long non-coding rnas that regulate and facilitate the process of x-inactivation and are important in the silencing of genes within the x chromosome that is being inactivated. these work in combination with tsix, which is non-coding rna that is an antisense which downregulates the effects of xist on the x chromosome in which it is expressed on the maternal x chromosome upon the start regulation of x-inactivation. these three rnas regulate the x-x pair in a cisorientation in order to be able to have both chromosomes available for inhibitory actions. tsix and xite have basic lncrnas functions in addition to x-inactivation and regulate the x-x pair in the transorientation. this ensures exclusive silencing for both x chromosomes. xite and tsix are both essential within the orientational directional processes in cis and trans as it is seen that without tsix and xite in trans it perturbs pairing and counting of genes. once the xist is turned off and no longer regulates the process, the tsix will slowly decrease in expression as well until both rnas are no longer being changed by xic. xite is the locus that harbors intergenic transcription start sites from hypersensitive sites of allelic crossovers/differences. when x-inactivation begins, the transcription of xite increases and signals for the downregulation of tsix in cisorientation, which is on the silent x chromosome, all while promoting the tsix persistence on the active x chromosome. xite also has major roles to play in the asymmetry of tsix expression and generates x chromosome inequality through moving and helping orient the chromosomes to be acted upon by the correct subsequent lncrna, either tsix or xist. neo-sex chromosomes and dosage compensation the monarch butterfly danaus plexippus belongs to the order lepidoptera and has 30 chromosomes one of which is a neo-sex chromosome which is the result of a fusion between one of the sex chromosomes and an autosome. a study using a combination of methods (hi-c assembly, coverage analysis and chip-seq) found that the neo-z segment exhibits complete dosage compensation which is achieved by increased transcription in zw females. interestingly, the ancestral z segment exhibits dosage balance with transcription levels being equal between both genders but less than the expected ancestral level, and this is achieved by decreased transcription in zz males.