This review focuses on those mouse mutations that cause an effect on the morphology, viability, and/or behavior of primordial germ cells (PGCs) and gonocytes at specific steps of their fetal development up to the start of spermatogenesis, a few days after birth. To restrict the area covered, mice with mutations that cause abnormal hormone levels or mutations of genes not expressed in germ cells that secondarily cause spermatogenic problems are not discussed. To make our literature search as comprehensive as possible, Pubmed was searched for “(primordial germ cells OR prospermatogonia OR prespermatogonia OR gonocytes OR spermatogonia ormeiosis or spermiogenesis or spermatogenesis) AND mouse AND (knockout or mutant or transgenic).” This search started at 2003 as mutants created earlier were already retrieved for a previous review. The resulting citations were then further selected for complete or partial arrests at the level of PGCs and/or gonocytes. Fifty-nine protein coding genes and two miRNA coding genes were found that arrest the development of PGCs and gonocytes at specific steps providing a better insight into the regulation of the development of these cells. As to be expected, often problems in fetal germ cell development have an effect on the fertility of the mice at adulthood.
Many gene mutations cause an arrest at specific developmental steps of mouse primordial germ cells and gonocytes, also called prospermatogonia, providing valuable clues for the regulation of their development.