|
|
Model |
Process | Features of the model |
Supporting data |
Conflicting data |
| Gene duplication | Duplicate function | Parental gene loss | Sex-biased gene location | New gene selection regime |
|
| (I) Escape from MSCI: genes are copied from X (or Z) to autosomes to replace the parental gene during meiotic sex chromosome inactivation in the heterogametic sex. Selective pressure should be strong on housekeeping genes that are needed in every cell, immediately after MSCI occurs, and new genes should keep parental function [11, 13, 58]. |  | Yes | Germline | No | Autosomes | Purifying selection | (i) Pattern of movement off the X [11–13, 15, 58]
(ii) Complementary expression of parental and new genes [16, 49]
(iii) Parental and new genes have same function (e.g., [59])
(iv) Export recapitulates sex chromosome history [60]
(v) There is a paucity of testis genes on the X [2, 61]
(vi) In mammals, the distribution of male-biased genes is highly depending on cell type [62, 63]. | (i) Genes copied from A to A also have male germline function [64]
(ii) New genes often have a different function (e.g., [65, 66])
(iii) New genes often evolve under positive selection [67–70]
(iv) New genes are lost [69]
(v) Export is still on going [11–13, 15, 58]
(vi) Paucity of somatic male-biased genes on the X [2, 61] |
|
| (II) Dosage compensation (DC): if there is a limit on how high you can express a gene and sex-biased expression is achieved increasing transcription [71], genes in the heteromorphic sex cannot achieve as high of an expression on the X (or Z) as on the autosomes and as a consequence an excess of highly expressed sex-biased genes on the autosomes might be observed [72]. |  | No | NA | No | Autosomes | Purifying selection | (i) Highly expressed sex-biased genes on the autosomes have been observed [72].
(ii) Paucity of male-biased genes on the X [2, 61] | (i) Pattern of movement off the X [11–13, 15, 58]
(ii) Genes copied from A to A also have male germline function [64] |
|
| (III) Escape from DC: in new sex chromosomes or chromosomal sections, genes might relocate to autosomes to attain dosage compensation. An efficient way is for the gene and regulatory region to copy to an autosome [14]. |  | Yes | Sex biased | Yes | Autosomes | No change in selection regime | (i) Male-biased genes are relocating from neo-X chromosomes to autosomes [4, 14, 15]. | |
|
| (IV) DC interference: it has been proposed that dosage compensation might interfere (A) with male-biased expression (i.e., interfere with further upregulation in males of DC genes [73]) or (B) with the evolution of tissue-specific expression (e.g., testis-specific expression; [50]) |  | Possibly | Sex biased/
Germline | No | NDC regions | NA | (i) Male-biased genes are locate in regions of the X that are not dosage compensated (i.e., NDC) [73]. | (i) Genes copied from A to A also have male germline function [64]
(ii) Export is still on going [11–13, 15, 58] |
|
| (V) Absence of DC: in the absence of dosage compensation, the heterogametic sex will have low expression of the genes on the X or Z chromosome [26, 28–30]. If you correct for this absence you expect not to observe a bias in the location of sexually dimorphic traits [74]. |  | No | NA | NA | X (Z) | NA | (i) Absence of dosage compensation has been observed in birds and Lepidoptera [32–35]. | |
|
| (VI) DC effects in the homogametic sex: the chromatin on the X chromosome might change in a way that the dosage compensated chromosome might now express higher than before in the homogametic sex. This might be interpreted as a lot of female biased genes on the X chromosome [36]. |  | No | NA | NA | X | NA | (i) X has higher transcription than the autosomes [36].
(ii) X has different chromatin even in the homogametic sex [75]. | (i) This does not apply to other lineages [30] |
|
| (VII) Sexual antagonism (SA) resolved through the evolution of modifiers of expression: sexual antagonistic variation (pink and blue alleles) will often appear on the X chromosome [27] and eventually modifiers of expression will evolve in one sex (e.g., females) to reduce expression of the gene leading to a dimorphic trait [27]. |  | No | Sex biased | NA | X (or Z) | NA | (i) Changes in expression are often in cis-regulatory regions [71]. | (i) There are a lot of genes with sex-biased expression generated through gene duplication [11–13, 15, 58, 64] or alternative splicing [76, 77].
(ii) Sex-biased genes evolve increasing expression [71].
(iii) SA seems to persist and not resolve [78]. |
|
| (VIII) SAXI: this model proposes that sexual antagonism leads to MSCI. If a gene duplicates from X to A, the autosomal copy might masculinize and the X copy might feminize because it spends 2/3 of its time in females. And finally leading to MSCI [79]. |  | Yes | Germline | No | X and autosomes | Specialization | (i) Pattern of movement off the X [11–13, 15, 58]
(ii) Complementary expression of parental and new genes [16, 49]
(iii) Export recapitulates sex chromosome history [60]
(iv) There is a paucity of testis genes on the X [2, 61] | (i) Paucity of somatic male-biased genes on the X [2, 61, 70]
(ii) Genes copied from A to A also have male germline function [64]
(iii) Export is still on going [11–13, 15, 58]
(iv) MSCI might be the outcome of the heterochromatization of unpaired chromatin [39, 53]. |
|
| (IX) SA resolution through gene duplication: intralocus sexual antagonism has been proposed to be resolved through duplication and the evolution of a female- and a male-biased gene [80, 81]. |  | Yes | Sex specific | No (Sex biased) | X and autosomes | Specialization | (i) There are a lot of genes with sex-biased expression generated through gene duplication [11–13, 15, 58, 64] | (i) Sex-biased genes generated through gene duplication are often tissue-specific genes [11–13, 15, 58, 64]. |
|
| (X) SA resolution through SA allele duplication: intralocus sexual antagonism might be strong in housekeeping genes because of the pressures of sex-specific tissues. This SA will be resolved with the duplication of one of the SA alleles and the evolution of tissue-specific transcription [17, 64, 69]. |  | Yes | Tissue specific (i.e., testis) | No | Autosomes | Positive selection (i.e., specialization or recurrent) | (i) Many testis-specific genes are generated through gene duplication [11–13, 15, 58, 64] from housekeeping genes from X but also from Autosomes.
(ii) New genes often have a different function [65, 66] or evolve under positive selection [67–69] or are lost [69].
(iii) Export is still on going [11–13, 15, 58].
(iv) Since the parental gene still expresses in both sexes, there is still a source of SA explaining why SA persists [78]. | (i) Parental and new genes have same function (e.g., [59]) |
|
| (XI) Gene duplication of a sex-biased gene under diversifying selection: the pressure of diversifying selection leads to balancing selection and gene duplication and the evolution of female- and male-biased genes from preexisting female- and male-biased genes [82, 83] |  | Yes | Sex specific | No (Sex biased) | X and autosomes | Positive selection (i.e., specialization or recurrent) | (i) Many sex-specific genes are generated through gene duplication from a preexisting sex-specific genes [82–85] | |
|
| (XII) SA and duplication to the Y chromosome: the Y chromosome will be a good location for genes with antagonistic effects between males and females [86, 87]. |  | Yes | Sex specific often tissue specific | No | Y (W) | Positive selection (i.e., specialization or recurrent) | (i) Y chromosome gains genes through time [86, 88]. | |
|
| (XIII) Random gain and loss of genes on the Y chromosome: neutral duplication and loss dynamics might lead to the gain of genes on the Y chromosome [88]. |  | Yes | Sex specific often tissue specific | Yes | Y (W) | NA | (i) Y chromosome losses but also gains male-biased genes through time often through DNA-mediated duplication [88]. | |
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