scholarly journals LFR Physically and Genetically Interacts With SWI/SNF Component SWI3B to Regulate Leaf Blade Development in Arabidopsis

2021 ◽  
Vol 12 ◽  
Author(s):  
Xiaowei Lin ◽  
Can Yuan ◽  
Bonan Zhu ◽  
Tingting Yuan ◽  
Xiaorong Li ◽  
...  
Keyword(s):  
Chromatin Remodeling ◽  
Apical Meristem ◽  
Peripheral Zone ◽  
Transcriptional Expression ◽  
Loss Of Function ◽  
Leaf Lamina ◽  
Protein Protein Interaction ◽  
Chromatin Remodeling Complex ◽  
Leaf Phenotype ◽  
Metabolism Enzyme

Leaves start to develop at the peripheral zone of the shoot apical meristem. Thereafter, symmetric and flattened leaf laminae are formed. These events are simultaneously regulated by auxin, transcription factors, and epigenetic regulatory factors. However, the relationships among these factors are not well known. In this study, we conducted protein-protein interaction assays to show that our previously reported Leaf and Flower Related (LFR) physically interacted with SWI3B, a component of the ATP-dependent chromatin remodeling SWI/SNF complex in Arabidopsis. The results of truncated analysis and transgenic complementation showed that the N-terminal domain (25–60 amino acids) of LFR was necessary for its interaction with SWI3B and was crucial for LFR functions in Arabidopsis leaf development. Genetic results showed that the artificial microRNA knockdown lines of SWI3B (SWI3B-amic) had a similar upward-curling leaf phenotype with that of LFR loss-of-function mutants. ChIP-qPCR assay was conducted to show that LFR and SWI3B co-targeted the promoters of YABBY1/FILAMENTOUS FLOWER (YAB1/FIL) and IAA carboxyl methyltransferase 1 (IAMT1), which were misexpressed in lfr and SWI3B-amic mutants. In addition, the association between LFR and the FIL and IAMT1 loci was partly hampered by the knockdown of SWI3B. These data suggest that LFR interacts with the chromatin-remodeling complex component, SWI3B, and influences the transcriptional expression of the important transcription factor, FIL, and the auxin metabolism enzyme, IAMT1, in flattened leaf lamina development.

scholarly journals Actin-Related Protein 4 Interacts with PIE1 and Regulates Gene Expression in Arabidopsis

Genes ◽  
2021 ◽  
Vol 12 (4) ◽  
pp. 520
Author(s):  
Wenfeng Nie ◽  
Jinyu Wang
Keyword(s):  
Gene Expression ◽  
Plant Growth ◽  
Chromatin Remodeling ◽  
Leaf Size ◽  
Early Flowering ◽  
Physical Interaction ◽  
Loss Of Function ◽  
Single Nucleotide Change ◽  
Chromatin Remodeling Complex ◽  
Related Proteins

As essential structural components of ATP-dependent chromatin-remodeling complex, the nucleolus-localized actin-related proteins (ARPs) play critical roles in many biological processes. Among them, ARP4 is identified as an integral subunit of chromatin remodeling complex SWR1, which is conserved in yeast, humans and plants. It was shown that RNAi mediated knock-down of Arabidopsis thaliana ARP4 (AtARP4) could affect plant development, specifically, leading to early flowering. However, so far, little is known about how ARP4 functions in the SWR1 complex in plant. Here, we identified a loss-of-function mutant of AtARP4 with a single nucleotide change from glycine to arginine, which had significantly smaller leaf size. The results from the split luciferase complementation imaging (LCI) and yeast two hybrid (Y2H) assays confirmed its physical interaction with the scaffold and catalytic subunit of SWR1 complex, photoperiod-independent early flowering 1 (PIE1). Furthermore, mutation of AtARP4 caused altered transcription response of hundreds of genes, in which the number of up-regulated differentially expressed genes (DEGs) was much larger than those down-regulated. Although most DEGs in atarp4 are related to plant defense and response to hormones such as salicylic acid, overall, it has less overlapping with other swr1 mutants and the hta9 hta11 double-mutant. In conclusion, our results reveal that AtARP4 is important for plant growth and such an effect is likely attributed to its repression on gene expression, typically at defense-related loci, thus providing some evidence for the coordination of plant growth and defense, while the regulatory patterns and mechanisms are distinctive from other SWR1 complex components.

Frameshift Variant in ARID2 in a Chilean Individual with Coffin–Siris Syndrome Phenotype

2021 ◽  
Author(s):  
Fernanda Martin Merlez ◽  
María González Zalazar ◽  
Silvia Castillo Taucher
Keyword(s):  
Chromatin Remodeling ◽  
Scalp Hair ◽  
Case Reports ◽  
Regulation Of Gene Expression ◽  
Loss Of Function ◽  
Disease Mechanism ◽  
Chromatin Remodeling Complex ◽  
Behavioral Abnormalities ◽  
Whole Exome ◽  
First Time

AbstractCoffin–Siris syndrome (CSS) is one of the several causes of intellectual disability (ID) and, since its first description, has posed diagnostic challenges given its variability and phenotypic overlap with other alterations of chromatin-remodeling-associated syndromes. It is genetically heterogeneous, and causative mutations are detected in less than 70% of cases. The different subtypes of the syndrome described to date are caused by mutations in genes that encode subunits of the SWI/SNF chromatin-remodeling complex, which plays an essential role in the regulation of gene expression during embryogenesis. Whole exome sequencing (WES) has allowed the identification of pathogenic mutations in these genes, including ARID2. ARID2 is one of the primary components of the SWI/SNF complex and has been associated with ID and phenotypes similar to CSS for the first time in 2015. Fifteen published case reports have identified loss-of-function mutations, suggesting that the underlying pathogenic disease mechanism is haploinsufficiency of ARID2.We herein presented the case of an 8-year-old Chilean girl with clinical suspicion of CSS, in whom a novel frameshift variant in ARID2 was identified by WES. She was the first reported case in Latin America to our knowledge and her phenotype displays the main clinical features suggestive of CSS described in other patients with ARID2 variants. However, she did not present behavioral abnormalities, a characteristic frequently reported in the majority of patients with ARID2 variants, and also had some features, such as sparse scalp hair, which is frequently reported as a manifestation of CSS, but is uncommon in this new group of patients.

scholarly journals Akirin Is Required for Muscle Function and Acts Through the TGF-β Sma/Mab Signaling Pathway in Caenorhabditis elegans Development

2019 ◽  
Vol 10 (1) ◽  
pp. 387-400 ◽  
Author(s):  
Richard Bowman ◽  
Nathan Balukoff ◽  
Amy Clemons ◽  
Emily Koury ◽  
Talitha Ford ◽  
...  
Keyword(s):  
Body Size ◽  
Caenorhabditis Elegans ◽  
Signaling Pathway ◽  
Chromatin Remodeling ◽  
Muscle Development ◽  
The Body ◽  
Model Systems ◽  
Loss Of Function ◽  
C Elegans ◽  
Chromatin Remodeling Complex

Akirin, a conserved metazoan protein, functions in muscle development in flies and mice. However, this was only tested in the rodent and fly model systems. Akirin was shown to act with chromatin remodeling complexes in transcription and was established as a downstream target of the NFκB pathway. Here we show a role for Caenorhabditis elegans Akirin/AKIR-1 in the muscle and body length regulation through a different pathway. Akirin localizes to somatic tissues throughout the body of C. elegans, including muscle nuclei. In agreement with its role in other model systems, Akirin loss of function mutants exhibit defects in muscle development in the embryo, as well as defects in movement and maintenance of muscle integrity in the C. elegans adult. We also have determined that Akirin acts downstream of the TGF-β Sma/Mab signaling pathway in controlling body size. Moreover, we found that the loss of Akirin resulted in an increase in autophagy markers, similar to mutants in the TGF-β Sma/Mab signaling pathway. In contrast to what is known in rodent and fly models, C. elegans Akirin does not act with the SWI/SNF chromatin-remodeling complex, and is instead involved with the NuRD chromatin remodeling complex in both movement and regulation of body size. Our studies define a novel developmental role (body size) and a new pathway (TGF-β Sma/Mab) for Akirin function, and confirmed its evolutionarily conserved function in muscle development in a new organism.

scholarly journals Crucial Roles for Interactions between MLL3/4 and INI1 in Nuclear Receptor Transactivation

2009 ◽  
Vol 23 (5) ◽  
pp. 610-619 ◽  
Author(s):  
Seunghee Lee ◽  
Dae-Hwan Kim ◽  
Young Hwa Goo ◽  
Young Chul Lee ◽  
Soo-Kyung Lee ◽  
...  
Keyword(s):  
Nuclear Receptor ◽  
Chromatin Remodeling ◽  
Target Genes ◽  
Mutational Analysis ◽  
Specific Protein ◽  
Transcriptional Coactivator ◽  
Set Domain ◽  
Protein Protein Interaction ◽  
Terminal Set ◽  
Chromatin Remodeling Complex

Abstract Nuclear receptor (NR) transactivation involves multiple coactivators, and the molecular basis for how these are functionally integrated needs to be determined to fully understand the NR action. Activating signal cointegrator-2 (ASC-2), a transcriptional coactivator of many NRs and transcription factors, forms a steady-state complex, ASCOM (for ASC-2 complex), which contains histone H3-lysine-4 (H3K4) methyltransferase MLL3 or its paralog MLL4. Here, we show that ASCOM requires a functional cross talk with the ATPase-dependent chromatin remodeling complex Swi/Snf for efficient NR transactivation. Our results reveal that ASCOM and Swi/Snf are tightly colocalized in the nucleus and that ASCOM and Swi/Snf promote each other’s binding to NR target genes. We further show that the C-terminal SET domain of MLL3 and MLL4 directly interacts with INI1, an integral subunit of Swi/Snf. Our mutational analysis demonstrates that this interaction underlies the mutual facilitation of ASCOM and Swi/Snf recruitment to NR target genes. Importantly, this study uncovers a specific protein-protein interaction as a novel venue to couple two distinct enzymatic coactivator complexes during NR transactivation.

scholarly journals Molecular genetics of atypical teratoid/rhabdoid tumors

2006 ◽  
Vol 20 (1) ◽  
pp. 1-7 ◽  
Author(s):  
Jaclyn A. Biegel
Keyword(s):  
Molecular Genetics ◽  
Chromatin Remodeling ◽  
Chromosome Band ◽  
Loss Of Function ◽  
Primary Tumors ◽  
Chromatin Remodeling Complex ◽  
Atypical Teratoid ◽  
Atypical Teratoid Rhabdoid Tumors ◽  
Rhabdoid Tumors ◽  
Infants And Young Children

Rhabdoid tumors are extremely aggressive malignancies that generally occur in infants and young children. The most common locations are the kidney and central nervous system (atypical teratoid/rhabdoid tumor [RT]), although RTs can also arise in most soft-tissue sites. Rhabdoid tumors in all anatomical locations have a similar molecular origin. Mutation or deletion of both copies of the hSNF5/INI1 gene that maps to chromosome band 22q11.2 is observed in approximately 70% of primary tumors. An additional 20 to 25% of tumors have reduced expression at the RNA or protein level, indicative of a loss-of-function event. The INI1 protein is a component of the SWI/SNF chromatin-remodeling complex. The complex is recruited to promoters of a large variety of genes involved in cell signaling, growth, and differentiation. This review summarizes what is currently known regarding the molecular genetics of RTs.

A Misexpression Study Examining Dorsal Thorax Formation in Drosophila melanogaster

Genetics ◽  
2002 ◽  
Vol 160 (3) ◽  
pp. 1035-1050
Author(s):  
María Teresa Peña-Rangel ◽  
Isabel Rodriguez ◽  
Juan Rafael Riesgo-Escovar
Keyword(s):  
Cell Cycle ◽  
Drosophila Melanogaster ◽  
Chromatin Remodeling ◽  
Cell Cycle Regulation ◽  
Transcriptional Control ◽  
Genetic Data ◽  
Loss Of Function ◽  
Functional Roles ◽  
Chromatin Remodeling Complex ◽  
Cycle Regulation

Abstract We studied thorax formation in Drosophila melanogaster using a misexpression screen with EP lines and thoracic Gal4 drivers that provide a genetically sensitized background. We identified 191 interacting lines showing alterations of thoracic bristles (number and/or location), thorax and scutellum malformations, lethality, or suppression of the thoracic phenotype used in the screen. We analyzed these lines and showed that known genes with different functional roles (selector, prepattern, proneural, cell cycle regulation, lineage restriction, signaling pathways, transcriptional control, and chromatin organization) are among the modifier lines. A few lines have previously been identified in thorax formation, but others, such as chromatin-remodeling complex genes, are novel. However, most of the interacting loci are uncharacterized, providing a wealth of new genetic data. We also describe one such novel line, poco pelo (ppo), where both misexpression and loss-of-function phenotypes are similar: loss of bristles and scutellum malformation.

scholarly journals Interplay of BAF and MLL4 promotes cell type-specific enhancer activation

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Young-Kwon Park ◽  
Ji-Eun Lee ◽  
Zhijiang Yan ◽  
Kaitlin McKernan ◽  
Tommy O’Haren ◽  
...  
Keyword(s):  
Cell Differentiation ◽  
Chromatin Remodeling ◽  
Direct Evidence ◽  
Cell Type ◽  
Chromatin Regulators ◽  
Chromatin Remodeling Complex ◽  
Histone H3k4 ◽  
Cell Type Specific ◽  
Pioneer Transcription Factor ◽  
Factor C

AbstractCell type-specific enhancers are activated by coordinated actions of lineage-determining transcription factors (LDTFs) and chromatin regulators. The SWI/SNF chromatin remodeling complex BAF and the histone H3K4 methyltransferase MLL4 (KMT2D) are both implicated in enhancer activation. However, the interplay between BAF and MLL4 in enhancer activation remains unclear. Using adipogenesis as a model system, we identify BAF as the major SWI/SNF complex that colocalizes with MLL4 and LDTFs on active enhancers and is required for cell differentiation. In contrast, the promoter enriched SWI/SNF complex PBAF is dispensable for adipogenesis. By depleting BAF subunits SMARCA4 (BRG1) and SMARCB1 (SNF5) as well as MLL4 in cells, we show that BAF and MLL4 reciprocally regulate each other’s binding on active enhancers before and during adipogenesis. By focusing on enhancer activation by the adipogenic pioneer transcription factor C/EBPβ without inducing cell differentiation, we provide direct evidence for an interdependent relationship between BAF and MLL4 in activating cell type-specific enhancers. Together, these findings reveal a positive feedback between BAF and MLL4 in promoting LDTF-dependent activation of cell type-specific enhancers.

scholarly journals The mammalian INO80 chromatin remodeling complex is required for replication stress recovery

2014 ◽  
Vol 42 (14) ◽  
pp. 9074-9086 ◽  
Author(s):  
Ivelina Vassileva ◽  
Iskra Yanakieva ◽  
Michaela Peycheva ◽  
Anastas Gospodinov ◽  
Boyka Anachkova
Keyword(s):  
Chromatin Remodeling ◽  
Replication Stress ◽  
Stress Recovery ◽  
Chromatin Remodeling Complex
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