14-3-3 protein Bmh1 triggers short-range compaction of mitotic chromosomes by recruiting sirtuin deacetylase Hst2

Abstract

Key Points:• 14-3-3 protein Bmh1 bridges the interaction of Hst2 with phosphorylated H3 tails • Hst2 is multiply phosphorylated on its unstructured C-terminal tail • The interaction of Bmh1 with Hst2 is cell cycle dependent • Hst2 phosphorylation enhances its enzymatic activity AbstractMitotic chromosome compaction is licensed by kinetochores in yeast. Recruitment of Aurora kinase B elicits a cascade of events starting with phosphorylation of H3 S10, which signals the recruitment of lysine deacetylase Hst2 and the removal of H4 K16ac. The unmasked H4 tails interact with the acidic patch of neighbouring nucleosomes to drive short-range compaction of chromatin. Here, we demonstrate that the interaction of Hst2 with H3 S10ph is mediated by 14-3-3 protein Bmh1. As a homodimer, Bmh1 binds simultaneously to H3 S10ph and the phosphorylated C-terminus of Hst2. The Hst2-Bmh1 interaction is cell cycle dependent, reaching its maximum in M phase. Furthermore, we show that phosphorylation of C-terminal residues of Hst2 stimulates its deacetylase activity. Hence, the data presented here identify Bmh1 as a key player in the mechanism of licensing of chromosome compaction in mitosis.

Non-essential kinetochore proteins contribute to meiotic chromosome condensation through polo-like kinase

“…In budding and fission yeasts, the kinetochore proteins, in particular the essential inner and central proteins, are also shown to promote chromosome condensation (Kruitwagen et al, 2018, Nakazawa et al, 2008. Subsequent studies revealed that this happens through kinetochoremediated centromeric and pericentromeric recruitment of several proteins including cohesins (Guacci et al, 1997, Lavoie et al, 2004, shugoshin (Peplowska et al, 2014, Kruitwagen et al, 2018, Yahya et al, 2020, 14-3-3 protein, Bmh1 (Jain et al, 2021) and enzymes such as aurora B kinase, Ipl1 (Giet et al, 2001, Petersen et al, 2003, Lavoie et al, 2004, polo-like kinase, Cdc5 (St. Pierre et al, 2009, Bazile et al, 2010, Leonard et al, 2015, Lamothe et al, 2020 and a histone deacetylase, Hst2 ( Wilkins et al, 2014, Kruitwagen et al, 2015, Jain et al, 2021.…”