A new pre-print is available, "Human spermatogonial stem cells retain states with a foetal-like signature", in which we demonstrate that the transcriptional heterogeneity of the undifferentiated spermatogonial compartment varies not only between species but across development - and conjecture that a transcriptional program particular to spermatogonial stem cells (SSCs), known as "state 0B", functionally opposes cellular proliferation and maintains the SSCs in a ready-to-react state. This program is maintained all the way from foetal development to adulthood in humans, but it's lost at birth in rodents. What this could mean is that in humans - a comparatively longer-lived species - there's a selective benefit to "not rushing". We conjecture the role of state 0B is to facilitate DNA repair before the SSCs commit to becoming mature sperm. This "slowing down" program could help maintain germline integrity across a longer reproductive life. For a shorter-lived species, in contrast, there's no time to lose (which is why, for instance, mice enter puberty practically at birth) so the "state 0B" program isn't required. You can read more here.