Unusual chromatin structure associated with monoparalogous transcription of the Babesia bovis ves multigene family

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• 作者：Yingling Huang^a ; ¹ ; Yu-Ping Xiao^a ; David R. Allred^a ; ^b ; ^{allredd@ufl.edu}
• 关键词：Antigenic variation ; Babesia bovis ; Chromatin remodeling ; Chromatin structure ; Nucleosome remodeling ; Promoter structure ; Transcription
• 刊名：International Journal for Parasitology
• 出版年：2013
• 出版时间：February, 2013
• 年：2013
• 卷：43
• 期：2
• 页码：163-172
• 全文大小：1135 K

文摘

Rapid antigenic variation in Babesia bovis involves the variant erythrocyte surface antigen-1 (VESA1), a heterodimeric protein with subunits encoded by two branches of the ves multigene family. The ves1¦Á and ves1¦Â gene pair encoding VESA1a and 1b, respectively, are transcribed in a monoparalogous manner from a single locus of active ves transcription (LAT), just one of many quasi-palindromic ves loci. To determine whether this organization plays a role in transcriptional regulation, chromatin structure was first assessed. Limited treatment of isolated nuclei with micrococcal nuclease to assay nucleosomal patterning revealed a periodicity of 156-159 bp in both bulk chromatin and specific gene coding regions. This pattern also was maintained in the intergenic regions (IGr) of non-transcribed ves genes. In contrast, the LAT IGr adopts a unique pattern, yielding an apparent cluster of five closely-spaced hypersensitive sites flanked by regions of reduced nucleosomal occupancy. ves loci fall into three patterns of overall sensitivity to micrococcal nuclease or DNase I digestion, with only the LAT being consistently very sensitive. Non-transcribed ves genes are inconsistent in their sensitivity to the two enzymatic probes. Non-linear DNA structure in chromatin was investigated to determine whether unique structure arising as a result of the quasi-palindromic nature of the LAT may effect transcriptional control. The in vitro capacity of ves IGr sequences to adopt stable higher-order DNA structure is demonstrated here, but the presence of such structure in vivo was not supported. Based upon these results a working model is proposed for the chromatin structural remodeling responsible for the sequential expression of ves multigene family members from divergently-organized loci.