Distinct mechanisms for delimiting expression of four Caenorhabditis elegans transcription factor genes encoding activators or repressors

2011 ◽  
Vol 286 (2) ◽  
pp. 95-107 ◽  
Author(s):  
Sophie Bamps ◽  
Julia Wirtz ◽  
Ian A. Hope
Keyword(s):  
Transcription Factor ◽  
Caenorhabditis Elegans ◽  
Transcription Factor Genes ◽  
Genes Encoding

scholarly journals Multiple layers of transcriptional regulation by PLZF in NKT-cell development

2016 ◽  
Vol 113 (27) ◽  
pp. 7602-7607 ◽  
Author(s):  
Ai-Ping Mao ◽  
Michael G. Constantinides ◽  
Rebecca Mathew ◽  
Zhixiang Zuo ◽  
Xiaoting Chen ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Zinc Finger ◽  
Molecular Mechanisms ◽  
Promyelocytic Leukemia ◽  
Transcriptional Program ◽  
T Helper ◽  
Nkt Cell ◽  
Btb Domain ◽  
Transcription Factor Genes ◽  
Genes Encoding

The transcription factor PLZF [promyelocytic leukemia zinc finger, encoded by zinc finger BTB domain containing 16 (Zbtb16)] is induced during the development of innate and innate-like lymphocytes to direct their acquisition of a T-helper effector program, but the molecular mechanisms involved are poorly understood. Using biotinylation-based ChIP-seq and microarray analysis of both natural killer T (NKT) cells and PLZF-transgenic thymocytes, we identified several layers of regulation of the innate-like NKT effector program. First, PLZF bound and regulated genes encoding cytokine receptors as well as homing and adhesion receptors; second, PLZF bound and activated T-helper–specific transcription factor genes that in turn control T-helper–specific programs; finally, PLZF bound and suppressed the transcription of Bach2, a potent general repressor of effector differentiation in naive T cells. These findings reveal the multilayered architecture of the transcriptional program recruited by PLZF and elucidate how a single transcription factor can drive the developmental acquisition of a broad effector program.

scholarly journals New Roles for the Heterochronic Transcription Factor LIN-29 in Cuticle Maintenance and Lipid Metabolism at the Larval-to-Adult Transition in Caenorhabditis elegans

Genetics ◽  
2020 ◽  
Vol 214 (3) ◽  
pp. 669-690 ◽  
Author(s):  
Patricia Abete-Luzi ◽  
Tetsunari Fukushige ◽  
Sijung Yun ◽  
Michael W. Krause ◽  
David M. Eisenmann
Keyword(s):  
Transcription Factor ◽  
Caenorhabditis Elegans ◽  
Regulation Of Gene Expression ◽  
Early Time ◽  
Temporal Regulation ◽  
Adult Transition ◽  
Link Type ◽  
Offspring Production ◽  
Genes Encoding ◽  
Time Specific

Temporal regulation of gene expression is a crucial aspect of metazoan development. In the roundworm Caenorhabditis elegans, the heterochronic pathway controls multiple developmental events in a time-specific manner. The most downstream effector of this pathway, the zinc-finger transcription factor LIN-29, acts in the last larval stage (L4) to regulate elements of the larval-to-adult switch. Here, we explore new LIN-29 targets and their implications for this developmental transition. We used RNA-sequencing to identify genes differentially expressed between animals misexpressing LIN-29 at an early time point and control animals. Among 230 LIN-29-activated genes, we found that genes encoding cuticle collagens were overrepresented. Interestingly, expression of lin-29 and some of these collagens was increased in adults with cuticle damage, suggesting a previously unknown function for LIN-29 in adult cuticle maintenance. On the other hand, genes involved in fat metabolism were enriched among 350 LIN-29-downregulated targets. We used mass spectrometry to assay lipid content in animals overexpressing LIN-29 and observed reduced fatty acid levels. Many LIN-29-repressed genes are normally expressed in the intestine, suggesting cell-nonautonomous regulation. We identified several LIN-29 upregulated genes encoding signaling molecules that may act as mediators in the regulation of intestinally expressed genes encoding fat metabolic enzymes and vitellogenins. Overall, our results support the model of LIN-29 as a major regulator of adult cuticle synthesis and integrity, and as the trigger for metabolic changes that take place at the important transition from rapid growth during larval life to slower growth and offspring production during adulthood.

scholarly journals Minireview: Transcriptional Regulation in Pancreatic Development

Endocrinology ◽  
2005 ◽  
Vol 146 (3) ◽  
pp. 1025-1034 ◽  
Author(s):  
Joel F. Habener ◽  
Daniel M. Kemp ◽  
Melissa K. Thomas
Keyword(s):  
Transcription Factor ◽  
Early Stage ◽  
Notch Signaling Pathway ◽  
Pancreas Development ◽  
Β Cells ◽  
Neurogenin 3 ◽  
Pancreatic Development ◽  
Transcription Factor Genes ◽  
Genes Encoding ◽  
Sequential Activation

Considerable progress has been made in the understanding of the sequential activation of signal transduction pathways and the expression of transcription factors during pancreas development. Much of this understanding has been obtained by analyses of the phenotypes of mice in which the expression of key genes has been disrupted (knockout mice). Knockout of the genes for Pdx1, Hlxb9, Isl1, or Hex results in an arrest of pancreas development at a very early stage (embryonic d 8–9). Disruption of genes encoding components of the Notch signaling pathway, e.g. Hes1 or neurogenin-3, abrogates development of the endocrine pancreas (islets of Langerhans). Disruption of transcription factor genes expressed more downstream in the developmental cascade (Beta2/NeuroD, Pax4, NKx2.2, and Nkx6.1) curtails the formation of insulin-producing β-cells. An understanding of the importance of transcription factor genes during pancreas development has provided insights into the pathogenesis of diabetes, in which the mass of insulin-producing β-cells is reduced.

scholarly journals XBX-1 Encodes a Dynein Light Intermediate Chain Required for Retrograde Intraflagellar Transport and Cilia Assembly in Caenorhabditis elegans

2003 ◽  
Vol 14 (5) ◽  
pp. 2057-2070 ◽  
Author(s):  
Jenny C. Schafer ◽  
Courtney J. Haycraft ◽  
James H. Thomas ◽  
Bradley K. Yoder ◽  
Peter Swoboda
Keyword(s):  
Transcription Factor ◽  
Caenorhabditis Elegans ◽  
Sensory Neurons ◽  
Intraflagellar Transport ◽  
Anterograde Transport ◽  
Behavioral Abnormalities ◽  
Genes Encoding ◽  
Intermediate Chain

Intraflagellar transport (IFT) is a process required for flagella and cilia assembly that describes the dynein and kinesin mediated movement of particles along axonemes that consists of an A and a B complex, defects in which disrupt retrograde and anterograde transport, respectively. Herein, we describe a novel Caenorhabditis elegans gene, xbx-1, that is required for retrograde IFT and shares homology with a mammalian dynein light intermediate chain (D2LIC). xbx-1 expression in ciliated sensory neurons is regulated by the transcription factor DAF-19, as demonstrated previously for genes encoding IFT complex B proteins. XBX-1 localizes to the base of the cilia and undergoes anterograde and retrograde movement along the axoneme. Disruption of xbx-1 results in cilia defects and causes behavioral abnormalities observed in other cilia mutants. Analysis of cilia in xbx-1 mutants reveals that they are shortened and have a bulb like structure in which IFT proteins accumulate. The role of XBX-1 in IFT was further confirmed by analyzing the effect that other IFT mutations have on XBX-1 localization and movement. In contrast to other IFT proteins, retrograde XBX-1 movement was detected in complex A mutants. Our results suggest that the DLIC protein XBX-1 functions together with the CHE-3 dynein in retrograde IFT, downstream of the complex A proteins.

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