scholarly journals The Drosophila Pioneer Factor Zelda Modulates the Nuclear Microenvironment of a Dorsal Target Enhancer to Potentiate Transcriptional Output

2019 ◽  
Vol 29 (8) ◽  
pp. 1387-1393.e5 ◽  
Author(s):  
Shigehiro Yamada ◽  
Peter H. Whitney ◽  
Shao-Kuei Huang ◽  
Elizabeth C. Eck ◽  
Hernan G. Garcia ◽  
...  
Keyword(s):  
Pioneer Factor ◽  
Transcriptional Output

scholarly journals The Drosophila pioneer factor Zelda modulates the nuclear microenvironment of a Dorsal target enhancer to potentiate transcriptional output

2018 ◽  
Author(s):  
Shigehiro Yamada ◽  
Peter H. Whitney ◽  
Shao-Kuei Huang ◽  
Elizabeth C. Eck ◽  
Hernan G. Garcia ◽  
...  
Keyword(s):  
Rna Polymerase Ii ◽  
Target Gene ◽  
Rate Increase ◽  
Imaging System ◽  
Effective Rate ◽  
Model System ◽  
Developmental Patterning ◽  
Pioneer Factor ◽  
Transcriptional Output

SummaryConnecting the developmental patterning of tissues to the mechanistic control of RNA polymerase II remains a long term goal of developmental biology. Many key elements have been identified in the establishment of spatial-temporal control of transcription in the early Drosophila embryo, a model system for transcriptional regulation. The dorsal/ventral axis of the Drosophila embryo is determined by the graded distribution of Dorsal (DL), a homologue of the NF-κB family of transcriptional activators found in humans [1,2]. A second maternally deposited factor, Zelda (ZLD), is uniformly distributed in the embryo and is thought to act as a pioneer factor, increasing enhancer accessibility for transcription factors such as DL [3–9]. Here we utilized the MS2 live imaging system to evaluate the expression of the DL target gene short gastrulation (sog) to better understand how a pioneer factor affects the kinetic parameters of transcription. Our experiments indicate that ZLD modifies probability of activation, the timing of this activation, and the rate at which transcription occurs. Our results further show that this effective rate increase is due to an increased accumulation of DL at the site of transcription, suggesting that transcription factor “hubs” induced by ZLD [10] functionally regulate transcription.

scholarly journals An Epigenetic Priming Mechanism Mediated by Nutrient Sensing Regulates Transcriptional Output

2020 ◽  
Author(s):  
Natalia Stec ◽  
Katja Doerfel ◽  
Kelly Hills-Muckey ◽  
Victoria M. Ettorre ◽  
Sevinc Ercan ◽  
...  
Keyword(s):  
Cell Fate ◽  
Transcriptional Activation ◽  
Nutrient Sensing ◽  
Pioneer Factor ◽  
Animal Size ◽  
Transcriptional Output ◽  
Transcriptional Induction ◽  
Target Gene Transcription ◽  
Subsequent Target ◽  
Gene Expression Levels

SummaryWhile precise tuning of gene expression levels is critical for most developmental pathways, the mechanisms by which the transcriptional output of dosage-sensitive molecules is established or modulated by the environment remain poorly understood. Here, we provide a mechanistic framework for how the conserved transcription factor BLMP-1/Blimp1 operates as a pioneer factor to decompact chromatin near its target loci hours before transcriptional activation and by doing so, regulates both the duration and amplitude of subsequent target gene transcription. This priming mechanism is genetically separable from the mechanisms that establish the timing of transcriptional induction and functions to canalize aspects of cell-fate specification, animal size regulation, and molting. A key feature of the BLMP-1-dependent transcriptional priming mechanism is that chromatin decompaction is initially established during embryogenesis and maintained throughout larval development by nutrient sensing. This anticipatory mechanism integrates transcriptional output with environmental conditions and is essential for resuming normal temporal patterning after animals exit nutrient-mediated developmental arrests.

scholarly journals Pioneer factor Foxa2 enables ligand-dependent activation of type II nuclear receptors FXR and LXRα

2021 ◽  
pp. 101291
Author(s):  
Jessica Kain ◽  
Xiaolong Wei ◽  
Nihal A. Reddy ◽  
Andrew J. Price ◽  
Claire Woods ◽  
...  
Keyword(s):  
Nuclear Receptors ◽  
Type Ii ◽  
Pioneer Factor

CLAMP regulates Zygotic Genome Activation in Drosophila embryos

Genetics ◽  
2021 ◽  
Author(s):  
Megan M Colonnetta ◽  
Juan E Abrahante ◽  
Paul Schedl ◽  
Daryl M Gohl ◽  
Girish Deshpande
Keyword(s):  
Temporal Dynamics ◽  
Embryonic Patterning ◽  
Zygotic Genome Activation ◽  
Promoter Sequences ◽  
Genome Wide ◽  
Zygotic Transcription ◽  
Pioneer Factor ◽  
Genome Activation ◽  
Drosophila Embryos ◽  
Zygotic Genome

Abstract Embryonic patterning is critically dependent on zygotic genome activation (ZGA). In Drosophila melanogaster embryos, the pioneer factor Zelda directs ZGA, possibly in conjunction with other factors. Here we have explored novel involvement of Chromatin-Linked Adapter for MSL Proteins (CLAMP) during ZGA. CLAMP binds thousands of sites genome-wide throughout early embryogenesis. Interestingly, CLAMP relocates to target promoter sequences across the genome when ZGA is initiated. Although there is a considerable overlap between CLAMP and Zelda binding sites, the proteins display distinct temporal dynamics. To assess whether CLAMP occupancy affects gene expression, we analyzed transcriptomes of embryos zygotically compromised for either clamp or zelda and found that transcript levels of many zygotically-activated genes are similarly affected. Importantly, compromising either clamp or zelda disrupted the expression of critical segmentation and sex determination genes bound by CLAMP (and Zelda). Furthermore, clamp knockdown embryos recapitulate other phenotypes observed in Zelda-depleted embryos, including nuclear division defects, centrosome aberrations, and a disorganized actomyosin network. Based on these data, we propose that CLAMP acts in concert with Zelda to regulate early zygotic transcription.

scholarly journals An evolutionarily 'young' lysine residue in histone H3 attenuates transcriptional output in Saccharomyces cerevisiae

2011 ◽  
Vol 25 (12) ◽  
pp. 1306-1319 ◽  
Author(s):  
E. M. Hyland ◽  
H. Molina ◽  
K. Poorey ◽  
C. Jie ◽  
Z. Xie ◽  
...  
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Histone H3 ◽  
Lysine Residue ◽  
Transcriptional Output

The Pattern Dependent Effects of Glucocorticoid Exposure on Prefrontal Cortex Transcriptional Output.

2010 ◽  
pp. P1-626-P1-626
Author(s):  
CL George ◽  
MA McKenna ◽  
JR Pooley ◽  
JA Douthwaite ◽  
SL Lightman ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Transcriptional Output

scholarly journals Temporal control of gene expression by the pioneer factor Zelda through transient interactions in hubs

2018 ◽  
Vol 9 (1) ◽  
Author(s):  
Jeremy Dufourt ◽  
Antonio Trullo ◽  
Jennifer Hunter ◽  
Carola Fernandez ◽  
Jorge Lazaro ◽  
...  
Keyword(s):  
Gene Expression ◽  
Temporal Control ◽  
Control Of Gene Expression ◽  
Pioneer Factor ◽  
Transient Interactions

scholarly journals Multi-enhancer transcriptional hubs confer phenotypic robustness

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Albert Tsai ◽  
Mariana RP Alves ◽  
Justin Crocker
Keyword(s):  
Transcription Factor ◽  
Drosophila Melanogaster ◽  
High Resolution ◽  
Elevated Temperatures ◽  
Regulatory Region ◽  
Deletion Allele ◽  
Genetic Perturbations ◽  
Transcription Sites ◽  
Phenotypic Robustness ◽  
Transcriptional Output

We previously showed in Drosophila melanogaster embryos that low-affinity Ultrabithorax (Ubx)-responsive shavenbaby (svb) enhancers drive expression using localized transcriptional environments and that active svb enhancers on different chromosomes tended to colocalize (Tsai et al., 2017). Here, we test the hypothesis that these multi-enhancer ‘hubs’ improve phenotypic resilience to stress by buffering against decreases in transcription factor concentrations and transcriptional output. Deleting a redundant enhancer from the svb locus led to reduced trichome numbers in embryos raised at elevated temperatures. Using high-resolution fluorescence microscopy, we observed lower Ubx concentration and transcriptional output in this deletion allele. Transcription sites of the full svb cis-regulatory region inserted into a different chromosome colocalized with the svb locus, increasing Ubx concentration, the transcriptional output of svb, and partially rescuing the phenotype. Thus, multiple enhancers could reinforce a local transcriptional hub to buffer against environmental stresses and genetic perturbations, providing a mechanism for phenotypical robustness.

scholarly journals Auxin requirements for a meristematic state in roots depend on a dual brassinosteroid function

2020 ◽  
Author(s):  
M. Ackerman-Lavert ◽  
Y. Fridman ◽  
R Matosevich ◽  
H Khandal ◽  
L. Friedlander ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Auxin Biosynthesis ◽  
Auxin Signaling ◽  
Critical Ratio ◽  
Dual Effect ◽  
Normal Morphology ◽  
Arabidopsis Root ◽  
Auxin Synthesis ◽  
Meristem Maintenance ◽  
Transcriptional Output

SummaryThe organization of the root meristem is maintained by a complex interplay between plant hormones signaling pathways that both interpret and determine their accumulation and distribution. Brassinosteroids (BR) and auxin signaling pathways control the number of meristematic cells in the Arabidopsis root, via an interaction that appears to involve contradicting molecular outcomes, with BR promoting auxin signaling input but also repressing its output. However, whether this seemingly incoherent effect is significant for meristem function is unclear. Here, we established that a dual effect of BR on auxin, with BR simultaneously promoting auxin biosynthesis and repressing auxin transcriptional output, is essential for meristem maintenance. Blocking BR-induced auxin synthesis resulted in rapid BR-mediated meristem loss. Conversely, plants with reduced BR levels were resistant to loss of auxin biosynthesis and these meristems maintained their normal morphology despite a 10-fold decrease in auxin levels. In agreement, injured root meristems which rely solely on local auxin synthesis, regenerated when both auxin and BR synthesis were inhibited. Use of BIN2 as a tool to selectively inhibit BR signaling, revealed meristems with distinct phenotypes depending on the perturbed tissue; meristem reminiscent of BR-deficient mutants or of high BR exposure. This enabled mapping BR-auxin interactions to the outer epidermis and lateral root cap tissues, and demonstrated the essentiality of BR signaling in these tissues for meristem maintenance. BR activity in internal tissues however, proved necessary to control BR homeostasis. Together, we demonstrate a basis for inter-tissue coordination and how a critical ratio between these hormones determines the meristematic state.

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