Skip to main content
. 2001 May;21(9):3244–3255. doi: 10.1128/MCB.21.9.3244-3255.2001

TABLE 1.

Phenotypes of Ink4c-null, Ink4d-null, and Ink4cd double-null male mice

Strain genotype Fertility Testis wt (mg)a Sperm countb Seminiferous tubule histochemistry Testosterone (ng/ml)b Leydig cells FSH (ng/ml)b
Wild type Fertile 124 ± 10.3 3.0 × 107 ± 0.8 × 107 Normal 13.5 ± 2.8 Normal 18.4 ± 3.6
Ink4c−/− Fertile 149 ± 12.7 4.5 × 107 ± 1.4 × 107 Normal 3.52 ± 1.3 Hyperplasticc 19.1 ± 5.1
Ink4d−/− Fertile 101 ± 18.4 2.0 × 107 ± 0.7 × 107 Meiotic delay, increased apoptosis 9.89 ± 2.8 Normal 35.8 ± 7.5
Ink4cd−/− Infertile 84.2 ± 9.9 0.44 × 107 ± 0.3 × 107 Pronounced meiotic delay, greatly increased apoptosis 2.84 ± 0.56 Hyperplasticc 45.0 ± 11
a

Testes from 6-month-old mice (wild type, n = 10; Ink4c null, n = 18; Ink4d null, n = 14; Ink4cd double null, n = 15). Data are averages ± standard deviations. 

b

Total number recovered per mouse using 10- to 14-week-old males. Numbers represent averages ± standard deviations from five or more animals of each genotype. 

c

Hyperplastic Leydig cells did not appear to differentiate based on the relatively low levels of histochemically detectable P450scc, the rate-limiting enzyme for steroid biogenesis.