| First Author | Fallon MA | Year | 2003 |
| Journal | Physiol Genomics | Volume | 14 |
| Issue | 2 | Pages | 95-106 |
| PubMed ID | 12847143 | Mgi Jnum | J:85119 |
| Mgi Id | MGI:2672147 | Doi | 10.1152/physiolgenomics.00151.2002 |
| Citation | Fallon MA, et al. (2003) The sld mutation is specific for sublingual salivary mucous cells and disrupts apomucin gene expression. Physiol Genomics 14(2):95-106 |
| abstractText | NFS/N-sld mice harbor a spontaneous autosomal recessive mutation, sld (sublingual gland differentiation arrest) and histologically display attenuated mucous cell expression in sublingual glands (Hayashi et al. Am J Pathol 132: 187-191, 1988). Because altered serous demilune cell expression is unknown, we determined the phenotypic expression of this cell type in mutants. Moreover, we evaluated whether absence of glycoconjugate staining in 3-day-old mutant glands is related to disruption in apomucin gene expression and/or to posttranslational glycosylation events. Serous cell differentiation is unaffected, determined morphologically and by serous cell marker expression (PSP, parotid secretory protein; and Dcpp, demilune cell and parotid protein). Conversely, apical granules in 'atypical' exocrine cells of mutant glands are PSP and mucin negative, but contain abundant SMGD (mucous granule marker). Age-related appearance of mucous cells is associated with expression of apomucin gene products, whereas SMGD expression is unaltered. 'Atypical' cells thus appear specified to a mucous cell fate but do not synthesize mucin glycoproteins unless selectively induced postnatally, indicating the sld mutation disrupts apomucin transcriptional regulation and/or decreases apomucin mRNA stability. |
