TAp73 deficiency causes a profound absence of developing and mature germ cells from the seminiferous epithelium. (A and B) Testis histology from p73KO and WT littermates at ages P20 (A) and P42 (B). H&E staining was used. Sexually mature 6-wk-old p73KO mice (B) show severe loss of developing germ cells and mature spermatozoa, creating “nearly empty” seminiferous tubules. Some variability in severity from tubule-to-tubule in a given KO mouse or among different mice was noted. (A and B, left) Whole testis with epididymis. (C) Testis histology from adult WT, p73KO, and isoform-specific ΔNp73KO and TAp73KO mice of similar age (7–10 wk). H&E staining was used. TAp73KO mice phenocopy global p73KO mice, whereas ΔNp73 deficiency does not affect testis morphology. (D) Severity of the testicular phenotype. Shown is a summary of all analyzed mice (6–10 wk) assessed by scoring H&E sections. p73KO (86%) and TAp73KO (100%) mice show medium-to-strong loss of developing and mature germ cells and a flat germ epithelium. In contrast, all ΔNp73KO mice have normal morphology. Asterisk: compared with its littermates, this 6-wk-old p73KO animal had small testis, which indicated delayed development. (E) p73 mRNA levels in different organs of 6–10-wk-old WT mice. qRT-PCR of all (pan) or TA/ΔN-specific isoforms was performed. TAp73 is the predominant isoform in testis (>100-fold higher than ΔNp73). n = 2–3 per organ, mean ± SD (error bars). *, P < 0.05 (t test). See also Fig. S1.