Abstract
Early diets in honeybees have effects on epigenome with consequences on their phenotype. Depending on the early larval diet, either royal jelly (RJ) or royal worker, 2 different female castes are generated from identical genomes, a long-lived queen with fully developed ovaries and a short-lived functionally sterile worker. To generate these prominent physiological and morphological differences between queen and worker, honeybees utilize epigenetic mechanisms which are controlled by nutritional input. These mechanisms include DNA methylation and histone post-translational modifications, mainly histone acetylation. In honeybee larvae, DNA methylation and histone acetylation may be differentially altered by RJ. This diet has biologically active ingredients with inhibitory effects on the de novo methyltransferase DNMT3A or the histone deacetylase 3 HDAC3 to create and maintain the epigenetic state necessary for developing larvae to generate a queen. DNMT and HDAC enzymes work together to induce the formation of a compacted chromatin structure, repressing transcription. Such dialog could be coordinated by their association with other epigenetic factors including the ubiquitin-like containing plant homeodomain (PHD) and really interesting new gene (RING) finger domains 1 (UHRF1). Through its multiple functional domains, UHRF1 acts as an epigenetic reader of both DNA methylation patterns and histone marks. The present review discusses the epigenetic regulation of honeybee's chromatin and how the early diets in honeybees can affect the DNA/histone modifying types of machinery that are necessary to stimulate the larvae to turn into either queen or worker. The review also looks at future directions in epigenetics mechanisms of honeybees, mainly the potential role of UHRF1 in these mechanisms.