Deviation from tri-bimaximal mixings in two types of inverted hierarchical neutrino mass models

An attempt is made to explore the possibility for deviations of solar mixing angle ($\theta_{12}$) from tri-bimaximal mixings, without sacrificing the predictions of maximal atmospheric mixing angle ($\theta_{23}=\pi/4$) and zero reactor angle ($\theta_{13}=0$). We find that the above conjecture can be automatically realised in the inverted hierarchical neutrino mass model having 2-3 symmetry, in the basis where charged lepton mass matrix is diagonal. For the observed ranges of $\bigtriangleup m^2_{21}$ and \bigtriangleup m^2_{23], we calculate the predictions on $\tan^2\theta_{12}=0.5, 0.45, 0.35$ for different input values of the parameters in the neutrino mass matrix. We also observe a possible crossing over from one type of inverted hierarchical model having same CP parity (Type-IHA) to other type having opposite CP parity (Type-IHB). Such neutrino mass matrices can be obtained from the canonical seesaw formula using diagonal form of Dirac neutrino mass matrix and non-diagonal texture of right-handed Majorana mass matrix, and may have important implications in model building using discrete as well as non-abelian symmetry groups.Comment: 13 pages, 7 figure

Deficient histone H3 propionylation by BRPF1-KAT6 complexes in neurodevelopmental disorders and cancer

Lysine acetyltransferase 6A (KAT6A) and its paralog KAT6B form stoichiometric complexes with bromodomain- and PHD finger-containing protein 1 (BRPF1) for acetylation of histone H3 at lysine 23 (H3K23). We report that these complexes also catalyze H3K23 propionylation in vitro and in vivo. Immunofluorescence microscopy and ATAC-See revealed the association of this modification with active chromatin. Brpf1 deletion obliterates the acylation in mouse embryos and fibroblasts. Moreover, we identify BRPF1 variants in 12 previously unidentified cases of syndromic intellectual disability and demonstrate that these cases and known BRPF1 variants impair H3K23 propionylation. Cardiac anomalies are present in a subset of the cases. H3K23 acylation is also impaired by cancer-derived somatic BRPF1 mutations. Valproate, vorinostat, propionate and butyrate promote H3K23 acylation. These results reveal the dual functionality of BRPF1-KAT6 complexes, shed light on mechanisms underlying related developmental disorders and various cancers, and suggest mutation-based therapy for medical conditions with deficient histone acylation

Deficient histone H3 propionylation by BRPF1-KAT6 complexes in neurodevelopmental disorders and cancer

Lysine acetyltransferase 6A (KAT6A) and its paralog KAT6B form stoichiometric complexes with bromodomain- and PHD finger-containing protein 1 (BRPF1) for acetylation of histone H3 at lysine 23 (H3K23). We report that these complexes also catalyze H3K23 propionylati