An African trypanosome variant surface glycoprotein gene whose expression is not activated by duplication

Area of Science:

• Molecular Biology
• Genetics
• Parasitology

Background:

• Trypanosoma brucei evades the host immune system by switching its variant surface glycoprotein (VSG).
• VSG gene expression is regulated by complex mechanisms, including gene duplication and transposition, but alternative pathways exist.

Purpose of the Study:

• To investigate the regulation of VSG gene expression in Trypanosoma brucei.
• To determine the role of flanking regions in VSG gene expression and switching.

Main Methods:

• Restriction mapping of VSG gene loci.
• Analysis of 5' and 3' flanking regions using restriction enzymes and BAL 31 nuclease.
• Comparison of gene structures in bloodstream and procyclic forms.

Main Results:

• Two copies of the VSG gene were identified with indistinguishable 5' flanking regions.
• Both VSG genes are located near chromosomal termini, indicated by restriction site-deficient regions and BAL 31 sensitivity.
• Length variation occurs in the 3' flanking regions, but the number of variants is conserved.

Conclusions:

• VSG gene expression is not solely regulated by duplication-transposition.
• Length variation in 3' flanking regions alone does not control VSG switching or expression.
• Constraints exist on the variability of 3' flanking regions, suggesting regulatory roles beyond simple length changes.