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Biology subjects

Jayakrishnan, M.

Publications and source records attributed to Jayakrishnan, M..

4 recordsLinked to original sources

Self-organization of Drosophila chromatin architecture in a cell-free system

Metazoan genomes are organized by folding of the nucleosome fiber into loops and domains that support long-range regulatory interactions. Although cohesin-mediated loop extrusion and architectural DNA-binding proteins are central to current models of genome organization, how these mechanisms integrate to generate higher-order structure remains incompletely understood. Early Drosophila melanogaster embryogenesis provides a unique window into the emergence of chromatin architecture, as rapid syncytial nuclear divisions occur largely in the absence of transcription. However, probing the mechanisms underlying this primordial folding in vivo is technically challenging. Here, we establish an in vitro system that reconstitutes complex chromatin using extracts from syncytial embryos. Nucleosome mapping and Micro-C analyses reveal that long-range interactions, including loops and topologically associating domains (TADs), emerge spontaneously from soluble extract components. While some structures resemble those observed in early embryos, others represent latent interaction potentials that are constrained in vivo. Focusing on the eve locus, we find that TAD formation is incompatible with a simple loop extrusion model and instead requires direct pairing of boundary elements mediated by the insulator protein Suppressor-of-hairy-wing Su(Hw). Together, our work demonstrates that key features of 3D genome organization can be reconstituted in a cell-free system and provides a tractable platform for mechanistic dissection of chromatin folding in Drosophila.

genomics↗

Dosage compensation defects due to roX RNA deletion are rescued by recalibration of X/autosome stoichiometry

Metazoa evolved regulatory networks to balance the expression of their sex chromosomes. In Drosophila, males have a single gene-rich X chromosome, whereas females have two. Balanced X/autosome expression is essential for viability, and in male flies is achieved by activation of genes on the X through the male-specific-lethal (MSL) dosage compensation complex (DCC). This ribonucleoprotein assembly contains long, non-coding roX RNAs. To dissect the functional requirements of roX in a cell-based system, we deleted the roX2 gene in male S2 cells and selected two independent lines lacking detectable roX RNA. In the absence of roX, the remaining MSL protein complex was unable to associate with known or newly identified binding sites and thus failed to activate transcription. Surprisingly, the X/autosome expression ratio appeared nevertheless compensated. Cytogenetic and genomic analyses revealed that both roX-deficient cell populations had acquired additional X chromosomes. Apparently, chromosome gains due to mis-segregation made up for the loss of DCC-mediated dosage compensation. Interestingly, ectopic expression of full-length roX2, but not of shortened derivatives, fully restored DCC binding and normalized the karyotype. These findings illustrate that X chromosome dosage compensation is critical for viability even in cultured cells and provide a striking example of rapid evolution under stringent selection. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=83 SRC="FIGDIR/small/707606v1_ufig1.gif" ALT="Figure 1"> View larger version (23K): org.highwire.dtl.DTLVardef@1bbf907org.highwire.dtl.DTLVardef@1da43a9org.highwire.dtl.DTLVardef@903326org.highwire.dtl.DTLVardef@10e3865_HPS_FORMAT_FIGEXP M_FIG C_FIG

molecular biology↗

KIF5B and Dynein regulate adhesion-dependent Golgi organization and microtubule acetylation

Cell-matrix adhesion regulates Golgi organization through Arf1-mediated dynein recruitment, maintaining its juxtanuclear localization. On loss of adhesion, Arf1 activation drops, causing loss of dynein, promoting differential disorganization of cis- vs trans-Golgi along microtubules. Golgi regulates microtubule nucleation and stability. In fibroblasts, acetylated tubulin levels drop on loss of adhesion, recovering on re-adhesion with time. Active Arf1 overexpression in preventing Golgi disorganization sustains microtubule acetylation, also seen in T24 bladder cancer cells. Active Arf1 binds KIF5B, recruiting it to the Golgi. KIF5B and dynein knockdown disorganize the Golgi as ministacks, with cis- and trans-Golgi. Dynein knockdown disrupts MTOC positioning, causing ministacks to disperse, preventing Golgi reorganization upon re-adhesion. Dispersed ministacks interestingly maintain microtubule acetylation in adherent and non-adherent cells. The joint KIF5B-dynein knockdown causes the Golgi to lose its ribbon morphology, becoming compact while keeping cis- and trans-Golgi together. This also causes a change in spreading, aspect ratio and migration of knockdown cells, which could be regulated by their Golgi phenotype. In evaluating adhesion-dependent Golgi organization, we reveal the Arf1-KIF5B-dynein crosstalk to regulate Golgi-dependent tubulin acetylation and cell function. SummaryKIF5B and dynein are vital microtubule-associated motors that drive organelle positioning and organization. Adhesion-dependent Arf1 activation mediates KIF5B and dyneins recruitment to the Golgi, regulating its organization and position. This, in turn, regulates microtubule acetylation levels, localization, and cellular functions.

cell biology↗

Genomic context-dependent histone H3K36 methylation by three Drosophila methyltransferases and implications for dedicated chromatin readers

Methylation of histone H3 at lysine 36 (H3K36me3) marks active chromatin. The mark is interpreted by epigenetic readers that assist transcription and safeguard the integrity of the chromatin fiber. The chromodomain protein MSL3 binds H3K36me3 to target X-chromosomal genes in male Drosophila for dosage compensation. The PWWP-domain protein JASPer recruits the JIL1 kinase to active chromatin on all chromosomes. Unexpectedly, depletion of K36me3 had variable, locus-specific effects on the interactions of those readers. This observation motivated a systematic and comprehensive study of K36 methylation in a defined cellular model. Contrasting prevailing models, we found that K36me1, K36me2 and K36me3 each represent independent chromatin states. A gene-centric view of the changing K36 methylation landscape upon depletion of the three methyltransferases Set2, NSD and Ash1 revealed local, context-specific methylation signatures. Set2 catalyzes K36me3 predominantly at transcriptionally active euchromatin. NSD places K36me2/3 at defined loci within pericentric heterochromatin and on weakly transcribed euchromatic genes. Ash1 deposits K36me1 at regions with enhancer signatures. The genome-wide mapping of MSL3 and JASPer suggested that they bind K36me2 in addition to K36me3, which was confirmed by direct affinity measurement. This dual specificity attracts the readers to a broader range of chromosomal locations and increases the robustness of their actions.

molecular biology↗