We scored the chimeric eyes for the presence or absence and the size of the retrolental mass, as this is the principal abnormality uniformly detectable in
Arf −/− mice at P1. A mass was often detectable in chimeric eyes, including several in which the
Arf −/− contribution was quite low (e.g., cornea, 5%; retina, 1%; RPE, 17%; and tail DNA, 19%)
(Fig. 3A) . Whereas the penetrance of the phenotype approaches 100% in
Arf −/− eyes,
14 only 14 of 26 eyes of 18 wild-type↔
Arf −/− chimeras had a mass. Further, it was unilateral in three mice in which the
Arf −/− contribution to the retina ranged from 1% to 28%. In two of the three,
Arf −/− cells contributed more to the retina in the eye with a mass (4.1% and 22.9%) than the eye without a mass (0.7% and 4.9%). Across the entire group, the presence of a retrolental mass was associated with a higher proportion of
Arf −/− cells in the tail, retina, cornea, and RPE
(Fig. 3B) . A threshold effect seemed evident as a mass was always present when greater than 18% of the cornea (
n = 8), 28% of the retina (
n = 6), 32% of the RPE (
n = 7), or 50% of the tail DNA (
n = 5) was
Arf −/−, whereas it was always absent when less than 5% of the cornea (
n = 6), 1% of the retina (
n = 2), 17% of the RPE (
n = 5), and 19% of the tail DNA (
n = 2) was derived from cells lacking
Arf. Among samples with a retrolental mass, the mass size (a marker of disease severity) was not significantly associated with the relative amount of
Arf −/− cells in the cornea (
P = 0.2799), retina (
P = 0.4593), RPE (
P = 0.3249), or tail DNA (
P = 0.6415). However, due to the relatively small sample size, the statistical power for detecting a difference was somewhat limited. We conclude that, although a PHPV-like eye disease can develop in eyes lacking
Arf in only a subset of cells, the abnormal phenotype can sometimes be suppressed in chimeric eyes containing relatively more wild-type cells.