scholarly journals Distinct Chromatin Configurations Regulate the Initiation and the Maintenance of hGH Gene Expression

2013 ◽  
Vol 33 (9) ◽  
pp. 1723-1734 ◽  
Author(s):  
Yugong Ho ◽  
Brian M. Shewchuk ◽  
Stephen A. Liebhaber ◽  
Nancy E. Cooke
Keyword(s):  
Gene Expression ◽  
Gene Activation ◽  
Adult Life ◽  
Human Pituitary ◽  
Conditional Deletion ◽  
Specific Subset ◽  
Mammalian Genes ◽  
Dnase I Hypersensitive Site ◽  
Target Promoter ◽  
Mammalian Gene Expression

For many mammalian genes, initiation of transcription during embryonic development must be subsequently sustained over extensive periods of adult life. It remains unclear whether maintenance of gene expression reflects the same set of pathways as are involved in initial gene activation. The human pituitary growth hormone ( hGH-N ) locus is activated in the differentiating somatotrope midway through embryogenesis by a multicomponent locus control region (LCR). DNase I-hypersensitive site I (HSI) of the LCR is essential to full developmental activation of the hGH-N locus. Here we demonstrate that conditional deletion of HSI from the active hGH locus in the adult pituitary effectively silences hGH-N expression. Analyses of chromatin structure and locus positioning demonstrate that a specific subset of the HSI functions active in the embryo retain their HSI dependence in the adult pituitary. These functions sustain engagement of the hGH locus with polymerase II (Pol II) factories, histone acetylation at the hGH-N promoter, and looping of the LCR to its target promoter. These data reveal that HSI is essential to both the maintenance and the initiation phases of gene expression. These observations contribute to our mechanistic understanding of how stable patterns of mammalian gene expression are established in a terminally differentiated cell.

Effects of TGFβ1 on gene expression in the HP75 human pituitary tumor cell line identified by gene expression profiling

Endocrine ◽  
2008 ◽  
Vol 33 (1) ◽  
pp. 62-76 ◽  
Author(s):  
Katharina H. Ruebel ◽  
Alexey A. Leontovich ◽  
Yoshinori Tanizaki ◽  
Long Jin ◽  
Gail A. Stilling ◽  
...  
Keyword(s):  
Gene Expression ◽  
Tumor Cell ◽  
Gene Expression Profiling ◽  
Cell Line ◽  
Expression Profiling ◽  
Pituitary Tumor ◽  
Tumor Cell Line ◽  
Human Pituitary ◽  
Human Pituitary Tumor ◽  
Pituitary Tumor Cell

scholarly journals Aspergillus nidulans wetA activates spore-specific gene expression.

1991 ◽  
Vol 11 (1) ◽  
pp. 55-62 ◽  
Author(s):  
M A Marshall ◽  
W E Timberlake
Keyword(s):  
Gene Expression ◽  
Cell Wall ◽  
Aspergillus Nidulans ◽  
Gene Activation ◽  
Regulatory Function ◽  
Specific Gene ◽  
Coding Region ◽  
Vegetative Cells ◽  
Mutant Strains ◽  
Late Stages

The Aspergillus nidulans wetA gene is required for synthesis of cell wall layers that make asexual spores (conidia) impermeable. In wetA mutant strains, conidia take up water and autolyze rather than undergoing the final stages of maturation. wetA is activated during conidiogenesis by sequential expression of the brlA and abaA regulatory genes. To determine whether wetA regulates expression of other sporulation-specific genes, its coding region was fused to a nutritionally regulated promoter that permits gene activation in vegetative cells (hyphae) under conditions that suppress conidiation. Expression of wetA in hyphae inhibited growth and caused excessive branching. It did not lead to activation of brlA or abaA but did cause accumulation of transcripts from genes that are normally expressed specifically during the late stages of conidiation and whose mRNAs are stored in mature spores. Thus, wetA directly or indirectly regulates expression of some spore-specific genes. At least one gene (wA), whose mRNA does not occur in spores but rather accumulates in the sporogenous phialide cells, was activated by wetA, suggesting that wetA may have a regulatory function in these cells as well as in spores. We propose that wetA is responsible for activating a set of genes whose products make up the final two conidial wall layers or direct their assembly and through this activity is responsible for acquisition of spore dormancy.

scholarly journals Symbiotic Gene Activation is Interrupted by Endocrine Disrupting Chemicals

2001 ◽  
Vol 1 ◽  
pp. 653-655 ◽  
Author(s):  
Jennifer E. Fox ◽  
Matthew E. Burow ◽  
John A. McLachlan
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Estrogen Receptors ◽  
Mammalian Cell Culture ◽  
Endocrine Disrupting Chemicals ◽  
Gene Activation ◽  
Symbiotic Gene ◽  
Endocrine Disrupting ◽  
Plant Chemicals ◽  
By Products

Endocrine disrupting chemicals (EDCs) include organochlorine pesticides, plastics manufacturing by-products, and certain herbicides[1]. These chemicals have been shown to disrupt hormonal signaling in exposed wildlife, lab animals, and mammalian cell culture by binding to estrogen receptors (ER-α and ER-β) and affecting the expression of estrogen responsive genes[2,3]. Additionally, certain plant chemicals, termed phytoestrogens, are also able to bind to estrogen receptors and modulate gene expression, and as such also may be considered EDCs[4]. One example of phytoestrogen action is genistein, a phytochemical produced by soybeans, binding estrogen receptors, and changing expression of estrogen responsive genes which certain studies have linked to a lower incidence of hormonally related cancers in Japanese populations[5]. Why would plants make compounds that are able to act as estrogens in the human body? Obviously, soybeans do not intentionally produce phytoestrogens to prevent breast cancer in Japanese women.

scholarly journals Global quantification of mammalian gene expression control

Nature ◽  
2011 ◽  
Vol 473 (7347) ◽  
pp. 337-342 ◽  
Author(s):  
Björn Schwanhäusser ◽  
Dorothea Busse ◽  
Na Li ◽  
Gunnar Dittmar ◽  
Johannes Schuchhardt ◽  
...  
Keyword(s):  
Gene Expression ◽  
Mammalian Gene ◽  
Expression Control ◽  
Gene Expression Control ◽  
Mammalian Gene Expression

scholarly journals Assessing the Conservation of Mammalian Gene Expression Using High-Density Exon Arrays

2007 ◽  
Vol 24 (7) ◽  
pp. 1577-1577
Author(s):  
Y. Xing ◽  
Z. Ouyang ◽  
K. Kapur ◽  
M. P. Scott ◽  
W. H. Wong
Keyword(s):  
Gene Expression ◽  
High Density ◽  
Exon Arrays ◽  
Mammalian Gene ◽  
Mammalian Gene Expression

scholarly journals HOS15 is a transcriptional corepressor of NPR1-mediated gene activation of plant immunity

2020 ◽  
Vol 117 (48) ◽  
pp. 30805-30815
Author(s):  
Mingzhe Shen ◽  
Chae Jin Lim ◽  
Junghoon Park ◽  
Jeong Eun Kim ◽  
Dongwon Baek ◽  
...  
Keyword(s):  
Gene Expression ◽  
Ubiquitin Ligase ◽  
Transcriptional Activation ◽  
Plant Immunity ◽  
Gene Activation ◽  
Transcriptional Corepressor ◽  
Defense Gene Expression ◽  
Dynamic Regulation ◽  
Defense Gene ◽  
Transcriptional Corepressors

Transcriptional regulation is a complex and pivotal process in living cells. HOS15 is a transcriptional corepressor. Although transcriptional repressors generally have been associated with inactive genes, increasing evidence indicates that, through poorly understood mechanisms, transcriptional corepressors also associate with actively transcribed genes. Here, we show that HOS15 is the substrate receptor for an SCF/CUL1 E3 ubiquitin ligase complex (SCFHOS15) that negatively regulates plant immunity by destabilizing transcriptional activation complexes containing NPR1 and associated transcriptional activators. In unchallenged conditions, HOS15 continuously eliminates NPR1 to prevent inappropriate defense gene expression. Upon defense activation, HOS15 preferentially associates with phosphorylated NPR1 to stimulate rapid degradation of transcriptionally active NPR1 and thus limit the extent of defense gene expression. Our findings indicate that HOS15-mediated ubiquitination and elimination of NPR1 produce effects contrary to those of CUL3-containing ubiquitin ligase that coactivate defense gene expression. Thus, HOS15 plays a key role in the dynamic regulation of pre- and postactivation host defense.

scholarly journals Shp2 in uterine stromal cells critically regulates on time embryo implantation and stromal decidualization by multiple pathways during early pregnancy

PLoS Genetics ◽  
2022 ◽  
Vol 18 (1) ◽  
pp. e1010018
Author(s):  
Jianghong Cheng ◽  
Jia Liang ◽  
Yingzhe Li ◽  
Xia Gao ◽  
Mengjun Ji ◽  
...  
Keyword(s):  
Gene Expression ◽  
Signaling Pathways ◽  
Stromal Cells ◽  
Embryo Implantation ◽  
Endometrial Stromal Cells ◽  
Conditional Deletion ◽  
Enhancer Binding Protein ◽  
Epithelial Remodeling ◽  
Multiple Signaling ◽  
Transcription 3

Approximately 75% of failed pregnancies are considered to be due to embryo implantation failure or defects. Nevertheless, the explicit signaling mechanisms governing this process have not yet been elucidated. Here, we found that conditional deletion of the Shp2 gene in mouse uterine stromal cells deferred embryo implantation and inhibited the decidualization of stromal cells, which led to embryonic developmental delay and to the death of numerous embryos mid-gestation, ultimately reducing female fertility. The absence of Shp2 in stromal cells increased the proliferation of endometrial epithelial cells, thereby disturbing endometrial epithelial remodeling. However, Shp2 deletion impaired the proliferation and polyploidization of stromal cells, which are distinct characteristics of decidualization. In human endometrial stromal cells (hESCs), Shp2 expression gradually increased during the decidualization process. Knockout of Shp2 blocked the decidual differentiation of hESCs, while Shp2 overexpression had the opposite effect. Shp2 knockout inhibited the proliferation of hESCs during decidualization. Whole gene expression profiling analysis of hESCs during the decidualization process showed that Shp2 deficiency disrupted many signaling transduction pathways and gene expression. Analyses of hESCs and mouse uterine tissues confirmed that the signaling pathways extracellular regulated protein kinases (ERK), protein kinase B (AKT), signal transducer and activator of transcription 3 (STAT3) and their downstream transcription factors CCAAT/enhancer binding protein β (C/EBPβ) and Forkhead box transcription factor O1 (FOXO-1) were involved in the Shp2 regulation of decidualization. In summary, these results demonstrate that Shp2 plays a crucial role in stromal decidualization by mediating and coordinating multiple signaling pathways in uterine stromal cells. Our discovery possibly provides a novel key regulator of embryo implantation and novel therapeutic target for pregnancy failure.

scholarly journals Mamo decodes hierarchical temporal gradients into terminal neuronal fate

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Ling-Yu Liu ◽  
Xi Long ◽  
Ching-Po Yang ◽  
Rosa L Miyares ◽  
Ken Sugino ◽  
...  
Keyword(s):  
Gene Expression ◽  
Rna Binding ◽  
Rna Binding Proteins ◽  
Neuronal Diversity ◽  
Temporal Expression ◽  
Identity Maintenance ◽  
Temporal Gene Expression ◽  
Neuronal Fate ◽  
Mammalian Genes ◽  
Post Transcriptional Regulation

Temporal patterning is a seminal method of expanding neuronal diversity. Here we unravel a mechanism decoding neural stem cell temporal gene expression and transforming it into discrete neuronal fates. This mechanism is characterized by hierarchical gene expression. First, Drosophila neuroblasts express opposing temporal gradients of RNA-binding proteins, Imp and Syp. These proteins promote or inhibit chinmo translation, yielding a descending neuronal gradient. Together, first and second-layer temporal factors define a temporal expression window of BTB-zinc finger nuclear protein, Mamo. The precise temporal induction of Mamo is achieved via both transcriptional and post-transcriptional regulation. Finally, Mamo is essential for the temporally defined, terminal identity of α’/β’ mushroom body neurons and identity maintenance. We describe a straightforward paradigm of temporal fate specification where diverse neuronal fates are defined via integrating multiple layers of gene regulation. The neurodevelopmental roles of orthologous/related mammalian genes suggest a fundamental conservation of this mechanism in brain development.

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