Skip Navigation

This Article
Right arrow Print PDF (4719K)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Commercial Re-use Guidelines
for Open Access NAR Content
Google Scholar
Right arrow Articles by Jones, J. M.
Right arrow Articles by Meisler, M. H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Jones, J. M.
Right arrow Articles by Meisler, M. H.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Nucleic Acids Research, 1989, Vol. 17, No. 16 6613-6623
© 1989

ENZYMOLOGY

A salivary amylase transgene is efficiently expressed in liver but not in parotid gland of transgenic mice

Julie M. Jones, Scott A. Keller, Linda C. Samuelson, Laurelee Osbora*, Michael P. Rosenberg1,+ and Miriam H. Meisler

Department of Human Genetics, University of Michigan Medical School Ann Arbor, Michigan 48109-0618 1Mammalian Genetics Laboratory, National Cancer Institute Frederick, MD, USA

Received May 1, 1989. Accepted July 17, 1989.

Two distinct mouse amylase cDNAs, corresponding to the genes Amy-1.1 and Amy-1.2, have been isolated from a YBR/KJ parotid cDNA library. A cosmid clone containing the intact Amy-1.1 gene from strain YBR/Ki, including both the parotid and liver promoters, was transferred to the germ line of C57BL/6J mice. Two independent transgenic lines were produced. The transferred genes are organized as a 4-copy autosomal locus in line Tg518 and an 8-copy Y-linked locus in line Tg2736. Serum of both transgenic lines contained high levels of the AMY1B isozyme encoded by the transferred gene. Transcripts were detected in liver and, at a lower level, in several other tissues including white and brown fat. The anticipated expression in parotid was not observed. Constructs containing 270 or 540 bp of the 5' flanking region of the parotid promoter, cloned upstream of the chloramphenicol acetyltransferase (CAT) structural gene, were also not expressed in transgenic mice. The results suggest that sequences located more than 5 kb upstream of the Amy-1 parotid promoter and/or more than 10 kb downstream from the structural gene are required for parotid-specific expression. The results also demonstrate that non-parotid sources can produce a normal level of AMY1 in serum. Liver is the probable source of AMY1 in serum of these transgenic mice.

* Present addresses: Squibb Institute for Medical Research, Princeton, NJ 08543, USA

+ Present addresses: Biogen, Cambridge, MA 02142, USA


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 JDRHome page
K.G. Ten Hagen and M.M. Balys
Low Levels of GRP-Ca Expression in Transgenic Mice
Journal of Dental Research, April 1, 2000; 79(4): 926 - 929.
[Abstract] [PDF]

Home page
 CROBMHome page
D. K. Ann, H. H. Lin, and E. Kousvelari
Regulation of Salivary-Gland-Specific Gene Expression
Critical Reviews in Oral Biology & Medicine, January 1, 1997; 8(3): 244 - 252.
[Abstract] [Full Text] [PDF]

Home page
 CROBMHome page
M. H. Meisler and C.-N. Ting
The Remarkable Evolutionary History of the Human Amylase Genes
Critical Reviews in Oral Biology & Medicine, January 1, 1993; 4(3): 503 - 509.
[Abstract] [Full Text] [PDF]

Home page
 Genes Dev.Home page
C N Ting, M P Rosenberg, C M Snow, L C Samuelson, and M H Meisler
Endogenous retroviral sequences are required for tissue-specific expression of a human salivary amylase gene.
Genes & Dev., August 1, 1992; 6(8): 1457 - 1465.
[Abstract] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.