Disruption of pr-set7 reduces levels of His4 K20 methylation. His4 K20 methylation does not correlate with gene activity.

Lysine-20-methylated His4 is localized to chromatin-dense and transcriptionally silent regions. There is an inverse correlation in the number and intensity of bands containing methyl His4-K20 and acetyl His4-K16. Methylation of His4 lysine 20 maintains silent chromatin, in part, by precluding neighbouring acetylation on the His4 tail.

Mutations in Iswi affect both cell viability and gene expression during development.

Replication-coupling assembly factor (RCAF) is a protein complex that facilitates the assembly of nucleosomes onto newly replicated DNA in vitro. RCAF is comprised of asf1, His3 and His4.

In male germ cells, acetylated His4 appears to correlate with the general activity state of the chromosome rather than to an X-specific dosage compensation mechanism. Loss of mle has no detectable effect on expression or localisation of acetylated His4.

The majority of replication-dependent histone gene transcripts are not polyadenylated and in addition two types of polyadenylated transcripts can be detected. A small proportion of the histone mRNAs bear a short poly(A) tail which is added to the 3' terminus of a partially degraded stem-loop structure. Polyadenylation signals can be located downstream of the stem-loop structure that can be used to generate mRNAs with a poly(A) tail.

The ATPase activity of Iswi is completely inhibited by each of the four histone tails (His2A, His2B, His3 and His4), results indicate a novel role for the flexible histone tails in chromatin remodeling by Iswi.

Male-specific lethal (MSL) proteins accumulate in a subregion of male nuclei (the X chromosome) beginning at late blastoderm stage. X chromosomal binding of the MSLs is observed throughout embryonic and larval development in both diploid and polytene tissues. His4 colocalises with the MSLs in embryos.

HIS4-Ac16 is bound to the polytene X chromosome, as seen by antibody staining.

Immunostaining of embryonic and larval stages demonstrates that His4, msl-1 and msl-3 are associated with the male X chromosome as early as gastrulation, while mle binding is not detected until the late embryonic/late larval stages.

His4 is first detected on the X chromosome at stage 8 following msl-2 expression.

Expression pattern and localisation of mle, msl-1, msl-2 and His4 proteins are determined and results suggest that the protein associated with the X chromosome and are interdependent since early embryogenesis.

Lys5 and Lys12 are utilised during deposition-related His4 diacetylation.

The gene products of mle, msl-1 bind to the male X chromosome in an identical pattern, and the binding sites of H4Ac16 acetylated form of the His4 product are largely coincident with the mle/msl-1 binding sites. This localisation of H4Ac16 protein is dependent on the dosage compensation regulatory pathway.

Both carnitine and butyrate compounds induce an accumulation of hyperacetylated H4 histones on chromatin.

Antisera to H4Ac16 label the euchromatic X chromosome through mitosis, but neither the X heterochromatin nor autosomes.

msl-1, like mle and H4Ac16 (an acetylated form of the His4 product), exhibits a wild type male localisation pattern in Sxl^- XX nuclei.

His4 protein is preferentially acetylated on Lys12 by HatB in vitro.

The codon bias of the histone genes from D.melanogaster and D.hydei illustrates that the generalisation that abundantly expressed genes have a high codon bias and low rates of silent substitution does not hold for the histone genes.

The position of the homologous histone gene repeats within the nuclei of early embryo cells has been investigated. The two homologous histone gene clusters are distinct and separate through all stages of the cell cycle up to nuclear cycle 13. During interphase of cycle 14, the two clusters colocalise with high frequency, and move from near the midline of the nucleus towards the apical side.

TATA complex formation on the Hsp70Bb core promoter shows sequence dependence at the TATA element, at the transcription start site and further downstream. Similar interactions contribute to TATA complexes formed on the Hsp26 and His4 promoters.

DNA replication of the 5kb histone gene repeating unit in tissue culture cells (Drosophila Kc cells) initiates at multiple sites located within the repeating unit. Several replication pause sites are located at 5' upstream regions of some histone genes.

DNaseI footprinting analysis reveals core histones His2A, His2B, His3 and His4 (but not His1) bind to the kni, Kr and Ubx minimal enhancer elements in a periodic manner.

His4 protein isoforms acetylated at lysine residues 5, 8, 12, or 16 have been shown to have distinct patterns of distribution in interphase polytene chromosomes from larvae.

The pattern of His4 protein acetylation has been studied.

The genomic organisation of the histone genes in D.hydei closely resembles that of D.melanogaster.

The D.virilis core histone genes (Dvir\His2B, Dvir\His3, Dvir\His4 and Dvir\His2A), are arranged in the same order and orientation as the D.melanogaster core histone genes (His2B, His3, His4 and His2A). However, the His1 gene that is located between His2B and His3 in D.melanogaster is not found between Dvir\His2B and Dvir\His3 in D.virilis.

The expression of HIS-C genes, including His4, during oogenesis has been studied, and compared to periods of DNA synthesis and actin expression during this developmental stage.

4.8kb and 5.0kb repeats containing the histone genes His1, His2A, His2B, His3 and His4 are present in all of the more than 20 D.melanogaster strains studied. The strains differ in the relative amounts of the two repeat types, with the 5.0kb repeat always present in equal or greater amounts than the 4.8kb repeat. The strains also differ in a number of far less abundant fragments containing histone gene sequences.

Encodes Histone H4. See HIS-C record.