Vol. 123, No. 1 (Supplement) 2018
Supplement abstract

How nuclear phospholipase C beta 1 can regulate gene transcription?

Roberta Fiume
Università di Bologna, DIBINEM, Bologna, Italia
Cristina Mazzetti
Università di Bologna, DIBINEM, Bologna, Italia
Alessandro Poli
INGM, INGM, Milano, Italia
Ester Orsini
Università di Bologna, DIBINEM, Bologna, Italia
Roberto Mambelli
Università di Bologna, DIBINEM, Bologna, Italia
Anna Maria Billi
Università di Bologna, DIBINEM, Bologna, Italia
Lucio Cocco
Università di Bologna, DIBINEM, Bologna, Italia

Published 2018-12-30

How to Cite

Fiume, R., Mazzetti, C., Poli, A., Orsini, E., Mambelli, R., Billi, A. M., & Cocco, L. (2018). How nuclear phospholipase C beta 1 can regulate gene transcription?. Italian Journal of Anatomy and Embryology, 123(1), 89. https://doi.org/10.13128/ijae-11393

Abstract

Since 80s the importance for nuclear phosphoinositides regulating enzymes has emerged, revealing that they are different and independent from the counterpart in the cytosol. While it is still not clear how phosphoinositides are presented in the nucleus nor how they are con- trolled, scientists have shown that their levels are changed in response to many different types of stimuli and that they are able to interact with and regulate proteins that are involved in nuclear functions such as transcription, mRNA processing and export and DNA conformation. Nuclear phospholipase C beta 1 (PLCβ1) has been shown to directly regulate cell cycle progres- sion, differentiation and gene expression in a variety of different cell types [1-4].

We used human acute myeloid leukaemia THP-1 cells to investigate a possible role of PLCβ1 in epigenetic signalling. Epigenetic signalling is a mechanism by which environmental stimuli can impact on both short and long term gene transcriptional output and thereby control cell fate decisions. Here we shown that PLCβ1 directly regulates histone methyltransferase and demethylase, and as consequence, histone tails profiles that lead to transcription factors acces- sibility at the promoter of key genes involved in acute myeloid leukaemia.

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