Synthesis of the modified thymine base, beta-d-glucosyl-hydroxymethyluracil or 
J, within telomeric DNA of Trypanosoma brucei correlates with the bloodstream 
form specific epigenetic silencing of telomeric variant surface glycoprotein 
genes involved in antigenic variation. In order to analyze the function of base 
J in the regulation of antigenic variation, we are characterizing the regulatory 
mechanism of J biosynthesis. We have recently proposed a model in which 
chromatin remodeling by a SWI2/SNF2-like protein (JBP2) regulates the 
developmental and de novo site-specific localization of J synthesis within 
bloodstream form trypanosome DNA. Consistent with this model, we now show that 
JBP2 (-/-) bloodstream form trypanosomes contain five-fold less base J and are 
unable to stimulate de novo J synthesis in newly generated telomeric arrays.