RT Journal Article
SR Electronic
T1 An exon DNA element modulates heterochromatin spreading in the master regulator for sexual commitment in malaria parasites
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 2020.06.26.163105
DO 10.1101/2020.06.26.163105
A1 Carlos Cordon-Obras
A1 Anna Barcons-Simon
A1 Christine Scheidig-Benatar
A1 Aurelie Claës
A1 Valentin Sabatet
A1 Damarys Loew
A1 Artur Scherf
YR 2020
UL http://biorxiv.org/content/early/2020/06/26/2020.06.26.163105.abstract
AB Heterochromatin is essential in all eukaryotes to maintain genome integrity, long-term gene repression and to help chromosome segregation during mitosis. However, heterochromatin regions must be restricted by boundary elements to avoid its spreading over actively transcribed loci. In Plasmodium falciparum, facultative heterochromatin is important to regulate parasite virulence, antigenic variation and transmission. However, the underlying molecular mechanisms regulating repressive regions remain unknown. To investigate this topic, we chose the ap2-g gene, which forms a strictly delimited and independent heterochromatin island. Using electrophoretic motility shift assay (EMSA) we identified an ap2-g exon element at the 3’ end binding nuclear protein complexes. Upon replacement of this region by a gfp gene, we observed a shift in the heterochromatin boundary resulting in HP1 (Heterochromatin Protein 1) spreading over ∼2 additional kb downstream. We used this DNA element to purify candidate proteins followed by proteomic analysis. The identified complexes were found to be enriched in RNA-binding proteins, pointing to a potential role of RNA in the regulation of the ap2-g 3’ heterochromatin boundary. Our results provide insight into the unexplored topic of heterochromatin biology in P. falciparum and identify a DNA element within the master regulator of sexual commitment modulating heterochromatin spreading.Competing Interest StatementThe authors have declared no competing interest.