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First published online 27 February 2007
doi: 10.1242/jcs.03412

Journal of Cell Science 120, 1072-1080 (2007)
Published by The Company of Biologists 2007
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Research Article

Epigenetic regulation of facultative heterochromatinisation in Planococcus citri via the Me(3)K9H3-HP1-Me(3)K20H4 pathway

Silvia Bongiorni1, Barbara Pasqualini1, Monia Taranta1, Prim B. Singh2 and Giorgio Prantera1,*

1 Department of Agrobiologia e Agrochimica, University of Tuscia, 01100 Viterbo, Italy
2 Division of Tumor Biology, Dept. of Immunology and Cell Biology, Forschungszentrum Borstel, 23845 Borstel, Germany

* Author for correspondence (e-mail: prantera{at}unitus.it)

Accepted 16 January 2007

Using RNA interference (RNAi) we have conducted a functional analysis of the HP1-like chromobox gene pchet2 during embryogenesis of the mealybug Planococcus citri. Knocking down pchet2 expression results in decondensation of the male-specific chromocenter that normally arises from the developmentally-regulated facultative heterochromatinisation of the paternal chromosome complement. Together with the disappearance of the chromocenter the staining levels of two associated histone modifications, tri-methylated lysine 9 of histone H3 [Me(3)K9H3] and tri-methylated lysine 20 of histone H4 [Me(3)K20H4], are reduced to undetectable levels. Embryos treated with double-stranded RNA (dsRNA) targeting pchet2 also exhibit chromosome abnormalities, such as aberrant chromosome condensation, and also the presence of metaphases that contain `lagging' chromosomes. We conclude that PCHET2 regulates chromosome behavior during metaphase and is a crucial component of a Me(3)K9H3-HP1-Me(3)K20H4 pathway involved in the facultative heterochromatinisation of the (imprinted) paternal chromosome set.

Key words: Facultative heterochromatin, Epigenetics, HP1, Histone modification, Genomic imprinting


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