Roles of transition nuclear proteins in spermiogenesis

• Published in: Chromosoma Vol. 111; no. 8; pp. 483 - 488
• Main Authors: Meistrich, Marvin L, Mohapatra, Bhagyalaxmi, Shirley, Cynthia R, Zhao, Ming
• Format: Journal Article
• Language: English
• Published: Austria Springer Nature B.V 01-05-2003
• Subjects: Animals; Chromatin; Chromosomal Proteins, Non-Histone - genetics; Chromosomal Proteins, Non-Histone - physiology; DNA damage; Histones; Mice; Mice, Knockout; Mutants; Nuclear Proteins - genetics; Nuclear Proteins - physiology; Phenotypes; Proteins; Proteolysis; Sperm; Spermatogenesis - physiology; Spermiogenesis
• ISSN: 0009-5915; 1432-0886
• DOI: 10.1007/s00412-002-0227-z

The transition nuclear proteins (TPs) constitute 90% of the chromatin basic proteins during the steps of spermiogenesis between histone removal and the deposition of the protamines. We first summarize the properties of the two major transition nuclear proteins, TP1 and TP2, and present concepts, based on their time of appearance in vivo and in vitro properties, regarding their roles. Distinct roles for the two TPs in histone displacement, sperm nuclear shaping, chromatin condensation, and maintenance of DNA integrity have been proposed. More definitive information on their roles in spermiogenesis has recently been obtained using mice with null mutations in the Tnp1 or Tnp2 genes for TP1 and TP2, respectively. In these mice, histone displacement and sperm nuclear shaping appear to progress quite normally. Spermatid nuclear condensation occurs, albeit in an abnormal fashion, and the mature sperm of the Tnp -null mutants are not as condensed as wild-type sperm. There is also evidence that sperm from these mutant mice contain an elevated level of DNA strand breaks. The mutant sperm showed several unexpected phenotypes, including a high incidence of configurational defects, such as heads bent back on midpieces, midpieces in hairpin configurations, coils, and clumps, other midpiece defects, reduced levels of proteolytic processing of protamine 2 during maturation, and reduced motility. The two TPs appear partly to compensate for each other as both Tnp1 - and Tnp2 -null mice were able to produce offspring, and appear to have largely overlapping functions as the two mutants had similar phenotypes.