EXPRESSION OF THE HELIX-LOOP-HELIX GENE ID3 DURING MURINE EMBRYONIC-DEVELOPMENT

被引：42

作者：

ELLMEIER, W ^{[1
]}

WEITH, A ^{[1
]}

机构：

[1] RES INST MOLEC PATHOL,A-1030 VIENNA,AUSTRIA

来源：

DEVELOPMENTAL DYNAMICS | 1995年 / 203卷 / 02期

关键词：

ID3; HELIX-LOOP-HELIX; MURINE DEVELOPMENT; IN SITU HYBRIDIZATION;

D O I：

10.1002/aja.1002030205

中图分类号：

R602 [外科病理学、解剖学]; R32 [人体形态学];

学科分类号：

100101 ;

摘要：

The family of dominant-negative helix-loop-helix (dnHLH) transcriptional modulators consists of four mammalian genes known to date: Id1, Id2, Id3 (Id3 was formerly designated HLH462 or HEIR1 or HLH1R21), and Id4. We have performed a detailed study of Id3 expression in mouse embryos in order to gain insight into the possible developmental control functions of this gene and to compare its expression to that of other mammalian dnHLH genes. Employing RNA in situ hybridization on sectioned mouse embryos of gestational stages E9.5-17.5 and neonatal head, we generally detected a high abundance of transcripts at early stages that gradually declined at most sites toward E15.5. Expression of Id3 in embryos was detected in brain, spinal cord, olfactory system, branchial arches, limbs, sclerotome, endocardiac cushions, the outer lining of the gut, lung, retina, the collecting system of the kidney, and in tooth anlagen. Although the abundance of mRNA decreased toward later stages in most tissues, it remained high in teeth and kidney. This expression pattern suggests that Id3 functions both in undifferentiated tissues and in organs which are in the process of differentiation. When compared to the expression of other dnHLH genes, it becomes obvious that the pattern of Id3 mainly coincides with that of Id1. This may reflect a partial redundancy in gene function. Furthermore, previous experiments suggested a mutually exclusive expression of the proto-oncogene N-myc an Id3. The results of the present study confirm these data. (C) 1995 Wiley-Liss, Inc.

引用

页码：163 / 173

页数：11

共 44 条

[1]

Aguzzi A., Wagner E.F., Williams R.L., Courtneidge S.A., Sympathetic hyperplasia and neuroblastomas in transgenic mice expressing polyoma middle T antigen, New Biol., 2, pp. 533-543, (1990)

[2]

Aguzzi A., Ellmeier W., Weith A., Dominant and recessive molecular changes in neuroblastomas, Brain Pathol., 2, pp. 195-208, (1992)

[3]

Bard J.B., The development of the mouse kidney‐embryogenesis writ small, Curr. Opin. Genet. Dev., 2, pp. 589-595, (1992)

[4]

Benezra R., Davis R.L., Lockshon D., Turner D.L., Weintraub H., The protein Id: a negative regulator of helix‐loop‐helix DNA binding proteins, Cell, 61, pp. 49-59, (1990)

[5]

Biggs J., Murphy E.V., Israel M.A., A human Id‐like helix‐loop‐helix protein expressed during early development, Proc. Natl. Acad. Sci. U.S.A., 89, pp. 1512-1516, (1992)

[6]

Campos-Ortega J.A., Jan Y.N., Genetic and molecular bases of neurogenesis in Drosophila melanogaster, Annu. Rev. Neurosci., 14, pp. 399-420, (1991)

[7]

Christy B.A., Sanders L.K., Lau L.F., Copeland N.G., Jenkins N.A., Nathans D., An Id‐related helix‐loop‐helix protein encoded by a growth factor‐inducible gene, Proc. Natl. Acad. Sci. U.S.A., 88, pp. 1815-1829, (1991)

[8]

Cordle S.R., Henderson E., Masuoka H., Weil P.A., Stem R., Pancreatic beta‐cell‐type‐specific transcription of the insulin gene is mediated by basic helix‐loop‐helix DNA‐binding proteins, Mol. Cell. Biol., 11, pp. 1734-1738, (1991)

[9]

Deed R.W., Bianchi S.M., Atherton G.T., Johnston D., Santibanez-Koref M., Murphy J.J., Norton J.D., An immediate early human gene encodes an Id‐like helix‐loop‐helix protein and is regulated by protein kinase C activation in diverse cell types, Oncogene, 8, pp. 599-607, (1993)

[10]

DePinho R.A., Legout E., Feldman L.B., Kohl N.E., Yancopoulos G.D., Alt F.W., Structure and expression of the murine N‐myc gene, Proc. Natl. Acad. Sci. U.S.A., 83, pp. 1827-1831, (1986)

← 1 2 3 4 5 →