They are contractile cells which contain actin filaments and are primarily involved in transport of spermatozoa through the tubules.

[3] Overall, PTM cells have a role in both maintaining the structure of the tubules and regulating spermatogenesis through cellular interaction.

These are detected in the lamina propria of the seminiferous tubule and immunohistochemical studies have shown functional distinctions between these layers.

For those SSCs destined to form differentiating progenitor A1 spermatogonia (and hence spermatozoa), this is initiated at a defined stage during the spermatogenic cycle.

[7] The precise location of SSCs throughout various staged cohorts of the seminiferous tubule determines their renewal function, to continuously produce progeny.

[1] Following this, GDNF binds GFRA1 on spermatogonial stem cells, and RET co-receptor (a transmembrane tyrosine kinase) is consequently signalled throughout all undifferentiated spermatogonia.

Thus, SFK signalling is upregulated and genes encoding key transcription factors (bcl6b, brachyury, Id4, Lhx1) become activated.

[2] PTMs become recognisable at 12 weeks gestation in humans, and 13.5 days post conception in mice.

Those becoming myoid cells would sit on a basement membrane surrounding the developing seminiferous tubules.

The main difficulty in studying the development of PTMs is the lack of a molecular marker specific to them that is visible during early differentiation of the testis.

[3] PTMs were first observed in 1901, when Claudius Regaud made a detailed study of the histology and physiology of the seminiferous tubules in rats.