Figure 1.

The Foxn1^lacZ allele causes postnatal thymic atrophy. The lacZ allele is indicated in all figures as “Z.” (A) Thymi from 5-week-old +/+, +/lacZ, +/nu, lacZ/lacZ, lacZ/nu, and nu/nu. Foxn1 dosage is closely correlated with postnatal thymus phenotype. Scale bar: 2 mm, applies to all parts of panel A. (B) Hematoxylin-and-eosin–stained paraffin sections of thymi from +/lacZ, +/nu, lacZ/lacZ, and lacZ/nu mice at 10 weeks. Thymus size was greatly reduced, and cortico-medullary architecture was dramatically disorganized in lacZ/lacZ and lacZ/nu thymus. An 18-month-old wild-type thymus is shown as an involuted thymus control. Scale bar in the top panel and bottom panel: 1 mm and 100 μm respectively, applies to all upper parts and lower parts in panel B. m indicates medulla; c, cortex. (C) Hematoxylin-and-eosin–stained sections of 3-week-old Foxn1^+/nude, Foxn1^cre/nude;R26R, and Foxn1^lacZ/nude thymi. Scale bar: 2 mm. Foxn1^cre/nude;R26R thymus showed a phenotype similar to Foxn1^+/nude, indicating that the presence of β-gal protein in TECs does not cause the phenotype associated with the Foxn1^lacZ allele. (D) Total thymocyte numbers in +/lacZ, lacZ/lacZ, and lacZ/nu thymi from newborn through 70 days after birth. Newborn thymocyte numbers were similar in +/lacZ and lacZ/lacZ, and increased logarithmically in the first week after birth; thymocyte number in lacZ/nu thymi was smaller due to haploinsufficiency of the nude allele, but paralleled the other 2 genotypes for the first week.