Harderian Gland Development and Degeneration in the Fgf10 -Deficient Heterozygous Mouse

• Published in: Journal of developmental biology 2024-06, Vol.12 (2), p.16
• Main Authors: Ikeda, Shiori, Sato, Keita, Fujita, Hirofumi, Ono-Minagi, Hitomi, Miyaishi, Satoru, Nohno, Tsutomu, Ohuchi, Hideyo
• Format: Article
• Language: English
• Subjects: Animals; Atrophy; B cells; Connective tissue; Connective tissues; Digital cameras; Embryos; Ethanol; Exocrine glands; eyes; Fgf10; Fibroblast growth factor 10; Fibroblast growth factors; Genes; Haploinsufficiency; Harderian gland; heterozygosity; Heterozygotes; histology; Hybridization; Laboratories; loss-of-function mutation; melanization; Mesenchyme; mice; Microscopy; mouse; Neomycin; Neonates; phenotype; Phenotypes; Phosphatase; Physiological aspects; postpartum period; RNA polymerase
• ISSN: 2221-3759; 2221-3759
• DOI: 10.3390/jdb12020016

The mouse Harderian gland (HG) is a secretory gland that covers the posterior portion of the eyeball, opening at the base of the nictitating membrane. The HG serves to protect the eye surface from infection with its secretions. Mice open their eyelids at about 2 weeks of age, and the development of the HG primordium mechanically opens the eye by pushing the eyeball from its rear. Therefore, when HG formation is disturbed, the eye exhibits enophthalmos (the slit-eye phenotype), and a line of heterozygous loss-of-function mice exhibits slit-eye due to the HG atrophy. However, it has not been clarified how and when HGs degenerate and atrophy in mice. In this study, we observed the HGs in embryonic (E13.5 to E19), postnatal (P0.5 to P18) and 74-week-old mice. We found that more than half of the mice had markedly degenerated HGs, often unilaterally. The degenerated HG tissue had a melanized appearance and was replaced by connective tissue, which was observed by P10. The development of HGs was delayed or disrupted in the similar proportion of embryos, as revealed via histology and the loss of HG-marker expression. In situ hybridization showed expression was observed in the Harderian mesenchyme in wild-type as well as in the HG-lacking heterozygote at E19. These results show that the haploinsufficiency causes delayed or defective HG development, often unilaterally from the unexpectedly early neonatal period.