Age-Dependent Retinoic Acid Regulation of Gene Expression Distinguishes the Cervical, Thoracic, Lumbar, and Sacral Spinal Cord Regions during Development

1999 ◽  
Vol 21 (2) ◽  
pp. 113-125 ◽  
Author(s):  
William W. Rubin ◽  
Anthony-Samuel LaMantia
Keyword(s):  
Gene Expression ◽  
Spinal Cord ◽  
Retinoic Acid ◽  
Regulation Of Gene Expression ◽  
Age Dependent ◽  
Spinal Cord Regions ◽  
Sacral Spinal Cord

scholarly journals Genome-wide H3K9 Acetylation Level Increases with Age-Dependent Senescence of Flag Leaf in Rice (Oryza sativa)

2021 ◽  
Author(s):  
Yu Zhang ◽  
Yanyun Li ◽  
Yuanyuan Zhang ◽  
Zeyu Zhang ◽  
Deyu Zhang ◽  
...  
Keyword(s):  
Gene Expression ◽  
Oryza Sativa ◽  
Leaf Senescence ◽  
Epigenetic Modification ◽  
Flag Leaf ◽  
Regulation Of Gene Expression ◽  
Leaf Aging ◽  
Genome Wide ◽  
Age Dependent ◽  
H3k9 Acetylation

Flag leaf senescence is an important biological process that drives the remobilization of nutrients to the growing organs of rice. Leaf senescence is controlled by genetic information via gene expression and epigenetic modification, but the precise mechanism is as of yet unclear. Here, we analyzed genome-wide acetylated lysine residue 9 of histone H3 (H3K9ac) enrichment by chromatin immunoprecipitation-sequencing (ChIP-seq) and examined its association with transcriptomes by RNA-seq during flag leaf aging in rice (Oryza sativa). We found that genome-wide H3K9 acetylation levels increased with age-dependent senescence in rice flag leaf, and there was a positive correlation between the density and breadth of H3K9ac and gene expression and transcript elongation. A set of 1,249 up-regulated, differentially expressed genes (DEGs) and 996 down-regulated DEGs showing a strong relationship between temporal changes in gene expression and gain/loss of H3K9ac was observed during rice flag leaf aging. We produced a landscape of H3K9 acetylation- modified gene expression targets that includes known senescence-associated genes, metabolism-related genes, as well as miRNA biosynthesis- related genes. Our findings reveal a complex regulatory network of metabolism- and senescence-related pathways mediated by H3K9ac and also elucidate patterns of H3K9ac-mediated regulation of gene expression during flag leaf aging in rice.

Combination strategies for repair, plasticity, and regeneration using regulation of gene expression during the chronic phase after spinal cord injury

Synapse ◽  
2011 ◽  
Vol 65 (12) ◽  
pp. 1255-1281 ◽  
Author(s):  
Christine G. Gerin ◽  
Ikenna C. Madueke ◽  
Tina Perkins ◽  
Seritta Hill ◽  
Kristin Smith ◽  
...  
Keyword(s):  
Gene Expression ◽  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Regulation Of Gene Expression ◽  
Chronic Phase ◽  
Combination Strategies ◽  
Cord Injury

scholarly journals A Retinoid-Resistant Acute Promyelocytic Leukemia Subclone Expresses a Dominant Negative PML-RARα Mutation

Blood ◽  
1997 ◽  
Vol 89 (12) ◽  
pp. 4282-4289 ◽  
Author(s):  
Wenlin Shao ◽  
Laura Benedetti ◽  
William W. Lamph ◽  
Clara Nervi ◽  
Wilson H. Miller
Keyword(s):  
Gene Expression ◽  
Retinoic Acid ◽  
Ligand Binding ◽  
Cell Line ◽  
Acute Promyelocytic Leukemia ◽  
Regulation Of Gene Expression ◽  
Promyelocytic Leukemia ◽  
Dominant Negative

Abstract The unique t(15; 17) of acute promyelocytic leukemia (APL) fuses the PML gene with the retinoic acid receptor α (RARα) gene. Although retinoic acid (RA) inhibits cell growth and induces differentiation in human APL cells, resistance to RA develops both in vitro and in patients. We have developed RA-resistant subclones of the human APL cell line, NB4, whose nuclear extracts display altered RA binding. In the RA-resistant subclone, R4, we find an absence of ligand binding of PML-RARα associated with a point mutation changing a leucine to proline in the ligand-binding domain of the fusion PML-RARα protein. In contrast to mutations in RARα found in retinoid-resistant HL60 cells, in this NB4 subclone, the coexpressed RARα remains wild-type. In vitro expression of a cloned PML-RARα with the observed mutation in R4 confirms that this amino acid change causes the loss of ligand binding, but the mutant PML-RARα protein retains the ability to heterodimerize with RXRα and thus to bind to retinoid response elements (RAREs). This leads to a dominant negative block of transcription from RAREs that is dose-dependent and not relieved by RA. An unrearranged RARα engineered with this mutation also lost ligand binding and inhibited transcription in a dominant negative manner. We then found that the mutant PML-RARα selectively alters regulation of gene expression in the R4 cell line. R4 cells have lost retinoid-regulation of RXRα and RARβ and the RA-induced loss of PML-RARα protein seen in NB4 cells, but retain retinoid-induction of CD18 and CD38. Thus, the R4 cell line provides data supporting the presence of an RARα-mediated pathway that is independent from gene expression induced or repressed by PML-RARα. The high level of retinoid resistance in vitro and in vivo of cells from some relapsed APL patients suggests similar molecular changes may occur clinically.

scholarly journals Enhancing enhancers: new complexities in the retinoid regulation of gene expression

2004 ◽  
Vol 383 (1) ◽  
Author(s):  
Chris P. F. REDFERN
Keyword(s):  
Gene Expression ◽  
Retinoic Acid ◽  
Regulation Of Gene Expression ◽  
Specific Expression ◽  
Response Element ◽  
Hormone Response Elements ◽  
Signalling Molecules ◽  
Biochemical Journal ◽  
Signalling Molecule ◽  
X Receptors

Retinoic acid is a signalling molecule central to morphogenesis and musculoskeletal development. It can exist in several isomeric forms, of which all-trans- and 9-cis-retinoic acid are thought to be the most relevant as signalling molecules. Retinoic acid regulates gene expression via RARs (retinoic acid receptors) working as heterodimers with RXRs (retinoid X receptors). RXRs also heterodimerize with other nuclear receptors. In this issue of the Biochemical Journal, Harris et al. have shown that an enhancer responsible for chondrocyte-specific expression of the col11a2 gene is itself regulated by a retinoic-acid-dependent interaction with RXRβ bound to a downstream response element. Thus, RXRs bound to hormone-response elements can regulate gene expression indirectly via interactions with tissue-specific enhancers. This study raises interesting questions about the nature of the response element, the RXRβ partner and the ligands able to influence col11a2 expression, and will provide a model system with which to understand tissue and ligand specificity of retinoid responses.

scholarly journals Transcriptional regulation of gene expression clusters in motor neurons following spinal cord injury

BMC Genomics ◽  
2010 ◽  
Vol 11 (1) ◽  
pp. 365 ◽  
Author(s):  
Jesper Ryge ◽  
Ole Winther ◽  
Jacob Wienecke ◽  
Albin Sandelin ◽  
Ann-Charlotte Westerdahl ◽  
...  
Keyword(s):  
Gene Expression ◽  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Transcriptional Regulation ◽  
Motor Neurons ◽  
Regulation Of Gene Expression ◽  
Cord Injury

Regulation of gene expression by corticoid hormones in the brain and spinal cord

1998 ◽  
Vol 65 (1-6) ◽  
pp. 253-272 ◽  
Author(s):  
Alejandro F. De Nicola ◽  
Monica Ferrini ◽  
Susana L. Gonzalez ◽  
Maria Claudia Gonzalez Deniselle ◽  
Claudia A. Grillo ◽  
...  
Keyword(s):  
Gene Expression ◽  
Spinal Cord ◽  
Regulation Of Gene Expression ◽  
Brain And Spinal Cord ◽  
The Brain

Retinoic Acid Regulation of Gene Expression in Adipocytes

2018 ◽  
pp. 431-454
Author(s):  
Donald B. Jump ◽  
Gerald J. Lepar ◽  
Ormond A. MacDougald
Keyword(s):  
Gene Expression ◽  
Retinoic Acid ◽  
Regulation Of Gene Expression
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