Codominant expression of genes coding for different sets of inducible salivary polypeptides associated with parotid hypertrophy in two inbred mouse strains

✍ Scribed by Remigio O. López-Solís; Ulrike Kemmerling

• Publisher: John Wiley and Sons
• Year: 2005
• Tongue: English
• Weight: 167 KB
• Volume: 95
• Category: Article
• ISSN: 0730-2312
• DOI: 10.1002/jcb.20390

✦ Synopsis

Abstract

Experimental mouse parotid hypertrophy has been associated with the expression of a number of isoproterenol‐induced salivary proline‐rich polypeptides (IISPs). Mouse salivary proline‐rich proteins (PRPs) have been mapped both to chromosomes 6 and 8. Recently, mice of two inbred strains (A/Snell and A.Swiss) have been found to differ drastically in the IISPs. In this study, mice of both strains were used for cross‐breeding experiments addressed to define the pattern of inheritance of the IISP phenotype and to establish whether the IISPs are coded on a single or on several chromosomes. The IISP phenotype of individual mice was assessed by sodium dodecyl sulfate–polyacrylamide gel electrophoresis (SDS–PAGE) of whole saliva collected after three daily stimulations by isoproterenol. Parental A/Snell and A.Swiss mice were homogeneous for distinctive strain‐associated IISP‐patterns. First filial generation (F1) mice obtained from the cross of A/Snell with A.Swiss mice expressed with no exception both the A/Snell and A.Swiss IISPs (coexpression). In the second filial generation (F2) both parental IISP phenotypes reappeared together with a majority of mice expressing the F1‐hybrid phenotype (1:2:1 ratio). Backcrosses of F1 × A/Snell and F1 × A.Swiss produced offsprings displaying the F1 and the corresponding parental phenotypes with a 1:1 ratio. No recombinants were observed among F2 mice or among mice resulting from backcrosses. Thus, genes coding for the IISPs that are expressed differentially in both mouse strains are located on the same chromosome, probably at the same locus (alleles) or at quite closely linked loci (nonalleles). © 2005 Wiley‐Liss, Inc.