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The sld mutation is specific for sublingual salivary mucous cells and disrupts apomucin gene expression

¹ University of Rochester Medical Center, Center for Oral Biology and the Department of Pharmacology and Physiology, Rochester, New York 14642
² Departments of Pediatric Dentistry
³ BioStructure and Function, University of Connecticut Health Center, School of Dental Medicine, Farmington, Connecticut 06030
⁴ University of Southern California, Division of Diagnostic Sciences, School of Dentistry, Los Angeles, California 90089

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.

salivary glands; exocrine cells; secretion; mucins; postnatal development

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