Display Settings:

Format

Send to:

Choose Destination
See comment in PubMed Commons below
Mol Microbiol. 2002 Nov;46(4):971-84.

A novel Myb-related protein involved in transcriptional activation of encystation genes in Giardia lamblia.

Author information

  • 1Department of Pathology, University of California at San Diego, School of Medicine, CA 92102-8416, USA.

Abstract

Giardia lamblia is an important human intestinal parasite that survives outside of the host by differentiation of trophozoites into infectious cysts. Transcriptional regulation is key for encystation gene expression, but the mechanisms are unknown. Giardia genome database searches identified a myb-like gene (gmyb2) whose expression increased during encystation. Epitope-tagged gMyb2 localized to both nuclei. DNA binding and mutation analysis showed that gMyb2 binds specifically to C(T/A)ACAG, a c-Myb-like target sequence in the promoters of encystation-induced genes encoding gMyb2, three cyst wall proteins and G6PI-B, a key enzyme in cyst wall polysaccharide biosynthesis. gMyb2 binding sites were not found in the upstream regions of 31 other giardial genes. Deletion of the putative gMyb2 binding site greatly reduced encystation-specific promoter activity of g6pi-b. Fusion of gMyb2 binding sites to the constitutive ran promoter or g6pi-b promoter deletion lacking the gMyb2 binding site in-duced encystation-specific expression. gMyb2 may play an important role in transcriptional regulation of encystation genes, and may help co-ordinate synthesis of cyst wall proteins and polysaccharide. gMyb2 is the first giardial transcription factor to be functionally identified and the first that is associated with upregulation of encystation genes. This work provides a model for study of differential gene regulation in early diverging eukaryotic organisms.

PMID:
12421304
[PubMed - indexed for MEDLINE]

Publication Types, MeSH Terms, Substances, Secondary Source ID, Grant Support

Publication Types

MeSH Terms

Substances

Secondary Source ID

Grant Support

PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Blackwell Publishing
    Loading ...
    Write to the Help Desk