The following points highlight the eight main criticisms for Lyon’s hypothesis.
Criticism # 1.
That XO, XXX, XY, XX etc. individual differ among themselves suggesting that the entire X chromosome is not genetically inactive. If it were so, an XX and XXX female would have had no difference at all.
From various chemical stigmata it seems that a part of the X, if not the entire length, is inactive.
Criticism # 2.
In fact, autoradiography shows late replication:
i) In long arm of the two Xs in human.
ii) In the short arm of cow and
iii) In half X’s in hamster.
Criticism # 3.
The XO tumer indicatingly suggest that the second X at least in its minor segments, is required for feminization and fertility.
Criticism # 4.
The inactivation of all but one X’s has minimized the drastic effect not only in X polysomics but also in minor deletion or even omition of an X as compared to the severity of cells autosomal trisomic or deletion.
Criticism # 5.
Natural selection mostly remove the abnormal cell lines from a mosaic individual in course of time as cited by Whittinghill (1970) in individuals mosaic in relation to Duchenne muscular dystrophy.
Criticism # 6.
The fact that structurally abnormal X, be it a ring-X or an iso-X, is invariably late replicating, goes against random differentiation concept.
Criticism # 7.
Ghosal (1975) contemplated phenomenon of Y chromosome differentiation.
In adult male, somatic cell of Chinese hamster (XY male), Taylor (1960), in human males (Y) (Lima-de-Faria, 1961), in mouse and hamster male (Y) — Y chromosome is late replicating.
Criticism # 8.
Mimicry between X and Y chromosome differentiation: A striking similarity exists in between the second X (this would be late X), of the female and the Y chromosome of the male in being both —
i) Late replicating in adult somatic cell,
ii) Early replicating in the mediotic gonadal cells.
iii) Earliness in pre-implanted embryo during post-zygotic mitosis and
iv) Lateness in post-implanted embryos continuing in adults and
v) With the postulation that X and Y chromosome evolved from an ancestral homologous pair, followed by
vi) Differential heterochromatinization thereby restricting the pairing segments, their behavioural mimicry palpable.
Sex chromatin differentiation is neither a monopoly of the mammalian female nor restricted to the X-chromosome. But such a phenomenon does exist in case of mammalian females, and, hence, for Y chromosomes too.
From the different biochemical and cytogenetic data so far established it can be inferred that:
(i) A major portion not the entire length of the X-chromosome is inactivated.
(ii) The Y chromosome mimics the inactive X in several aspects.
(iii) The specific fractions complexed with heterochromatic segments of inactive X may interfere with the transcription process.
