Reprogramming histone modification patterns to coordinate gene expression in early zebrafish embryos

AbstractThe left-right symmetry breaking of vertebrate embryos requires fluid flow (called nodal flow in zebrafish). However, the molecular mechanisms that mediate the asymmetric gene expression regulation under nodal flow remain elusive. In this paper, we report that heat shock factor 1 (HSF1) is asymmetrically activated in the Kuppfer’s vesicle at the early stage of zebrafish embryos in the presence of nodal flow. Deficiency in HSF1 expression caused a significant situs inversus and disrupted gene expression asymmetry of nodal signaling proteins in zebrafish embryos. Further studies demonstrated that HSF1 could be immediately activated by fluid shear stress. The mechanical sensation ability of HSF1 is conserved in a variety of mechanical stimuli in different cell types. Moreover, cilia and the Ca2+-Akt signaling axis are essential for the activation of HSF1 under mechanical stress in vitro and in vivo. Considering the conserved expression of HSF1 in organisms, these findings unveil a fundamental mechanism of gene expression regulation triggered by mechanical clues during embryonic development and other physiological and pathological transformations.

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Pluripotency factors select gene expression repertoire at Zygotic Genome Activation

10.1101/2020.02.16.949362 ◽

2020 ◽

Cited By ~ 1

Author(s):

Meijiang Gao ◽

Marina Veil ◽

Marcus Rosenblatt ◽

Anna Gebhard ◽

Helge Hass ◽

...

Keyword(s):

Gene Expression ◽

Transcription Factors ◽

Early Gene ◽

Zebrafish Embryos ◽

Fate Specification ◽

Pluripotency Factors ◽

Zygotic Transcription ◽

Simultaneous Loss ◽

Genome Activation ◽

Zygotic Genome

AbstractAwakening of zygotic transcription in animal embryos relies on maternal pioneer transcription factors. The interplay of global and specific functions of these proteins remains poorly understood. Here, we analyzed nucleosome positioning, H3K27 acetylation, transcription, and gastrulation rates in zebrafish embryos lacking pluripotency factors Pou5f3 and Sox19b. We show that the bulk transcriptional onset does not require Sox19b and Pou5f3, but is sensitive to their balance. Pou5f3 docks H3K27ac on the enhancers of genes involved in gastrulation and ventral fate specification. Sox19b facilitates Pou5f3 access to one-third of these enhancers. The genes regulating mesendodermal and dorsal fates are primed for activation independently on Pou5f3 and Sox19b. Strikingly, the loss of either factor results in activation of silent enhancers; simultaneous loss of both leads to premature expression of differentiation genes. Our results uncover how independent activities of maternal Pou5f3 and Sox19b add up or antagonize to determine the early gene expression repertoire.

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Gene expression profile of zebrafish exposed to hypoxia during development

Physiological Genomics ◽

10.1152/physiolgenomics.00128.2002 ◽

2003 ◽

Vol 13 (2) ◽

pp. 97-106 ◽

Cited By ~ 185

Author(s):

Christopher Ton ◽

Dimitri Stamatiou ◽

Choong-Chin Liew

Keyword(s):

Gene Expression ◽

Gene Expression Profile ◽

Cdna Microarray ◽

Expression Profile ◽

Clinical Implications ◽

Zebrafish Embryos ◽

Hypoxic Stress ◽

Microarray Technology ◽

Adaptive Responses ◽

Low Oxygen

Understanding how vertebrates respond to hypoxia can have important clinical implications. Fish have evolved the ability to survive long exposure to low oxygen levels. However, little is known about the specific changes in gene expression that result from hypoxia. In this study we used a zebrafish cDNA microarray to examine the expression of >4,500 genes in zebrafish embryos exposed to 24 h of hypoxia during development. We tested the hypotheses that hypoxia changes gene expression profile of the zebrafish embryos and that these changes can be reverted by reexposure to a normoxic (20.8% O2) environment. Our data were consistent with both of these hypotheses: indicating that zebrafish embryos undergo adaptive changes in gene expression in response to hypoxia. Our study provides a striking genetic portrait of the zebrafish embryos’ adaptive responses to hypoxic stress and demonstrates the utility of the microarray technology as a tool for analyzing complex developmental processes in the zebrafish.

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