| Spermatid | |
|---|---|
 Germinal epithelium of thetesticle. 1:basal lamina 2:spermatogonia 3:spermatocyte 1st order 4: spermatocyte 2nd order 5: spermatid 6: mature spermatid 7:Sertoli cell 8:tight junction (blood testis barrier) | |
 | |
| Identifiers | |
| MeSH | D013087 |
| FMA | 72294 |
| Anatomical terminology | |
Thespermatid is thehaploid malegametid that results from division of secondaryspermatocytes. As a result ofmeiosis, each spermatid contains only half of the genetic material present in the original primary spermatocyte.
Spermatids are connected by cytoplasmic material and have superfluous cytoplasmic material around their nuclei.
When formed,early round spermatids must undergo further maturational events to develop intospermatozoa, a process termedspermiogenesis (also termedspermeteliosis).
The spermatids begin to grow a living thread, develop a thickened mid-piece where themitochondria become localised, and form anacrosome. Spermatid DNA also undergoes packaging, becoming highly condensed. The DNA is packaged firstly with specific nuclear basic proteins, which are subsequently replaced withprotamines during spermatid elongation. The resultant tightly packedchromatin is transcriptionally inactive.
In 2016 scientists atNanjing Medical University claimed they had produced cells resembling mouse spermatids artificially fromstem cells. They injected these spermatids into mouse eggs and produced pups.[1]
During spermatidhaploidgenome remodeling, the majority ofhistones are replaced byprotamines, and theDNA is compacted. During this compaction, transient single- and double-strand breaks are introduced into the sperm DNA.[2] The conventionalnon-homologous end joining pathway for repairing double-strand breaks is not available for elongated spermatids. However, spermatids can carry out limited repair of exogenous and programmed double-strand breaks using an alternative error-prone non-homologous end joining repair pathway.[3] If DNA strand breaks persist in mature sperm, the result can be increased sperm DNA fragmentation which is associated with impaired fertility and an increased incidence of miscarriage.[4]
As postmeioticgerm cells develop to maturesperm they progressively lose the ability to repairDNA damage that may then accumulate and be transmitted to thezygote and ultimately the embryo.[5] In particular, therepair of DNA double-strand breaks by thenon-homologous end joining pathway, although present in round spermatids, appears to be lost as they develop into elongated spermatids.[6]
.svg)
List of distinct cell types in the adult human body