scholarly journals PEAPOD limits developmental plasticity in Arabidopsis

2017 ◽  
Author(s):  
Derek W. R. White
Keyword(s):  
Transcriptional Activation ◽  
Developmental Plasticity ◽  
Higher Plants ◽  
Hormone Activity ◽  
Cambial Cell ◽  
Light Signalling ◽  
Regulatory Complex ◽  
Hormone Responses ◽  
Delayed Flowering ◽  
Developmental Responses

AbstractHigher plants utilise developmental plasticity to adapt to changes in the environment, especially to variations in light. Much of this change in growth and development involves the light-mediated regulation of multiple hormone pathways. However, despite considerable progress towards understanding the molecular processes controlling light signalling and hormone activity, regulatory mechanisms preventing exaggerated plant developmental responses are not well understood. Here I report that the PPD regulatory complex has a crucial role in limiting developmental plasticity in Arabidopsis. Reductions in PPD or KIX8/9 gene expression resulted in; tolerance to ABA inhibition of seed germination, hypocotyl elongation, increases in stomata on hypocotyls, cambial cell proliferation and seed weight, and delayed flowering. Transcript profiling and analyses of hormone responses and genetic interactions established PPD modulates developmental plasticity, mainly by a combination of transcriptional activation and repression of genes controlling CRY/PHY light signalling and ABA, auxin, brassinosteroid, cytokinin and gibberellin homeostasis.

Developmental Plasticity and Evolution

2003 ◽  
Author(s):  
Mary Jane West-Eberhard
Keyword(s):  
Adaptive Evolution ◽  
Evolutionary Biology ◽  
Developmental Plasticity ◽  
Higher Plants ◽  
Critical Discussion ◽  
Physiological Adaptation ◽  
Modular Organization ◽  
Random Mutation ◽  
Environmental Induction ◽  
Development And Evolution

The first comprehensive synthesis on development and evolution: it applies to all aspects of development, at all levels of organization and in all organisms, taking advantage of modern findings on behavior, genetics, endocrinology, molecular biology, evolutionary theory and phylogenetics to show the connections between developmental mechanisms and evolutionary change. This book solves key problems that have impeded a definitive synthesis in the past. It uses new concepts and specific examples to show how to relate environmentally sensitive development to the genetic theory of adaptive evolution and to explain major patterns of change. In this book development includes not only embryology and the ontogeny of morphology, sometimes portrayed inadequately as governed by "regulatory genes," but also behavioral development and physiological adaptation, where plasticity is mediated by genetically complex mechanisms like hormones and learning. The book shows how the universal qualities of phenotypes--modular organization and plasticity--facilitate both integration and change. Here you will learn why it is wrong to describe organisms as genetically programmed; why environmental induction is likely to be more important in evolution than random mutation; and why it is crucial to consider both selection and developmental mechanism in explanations of adaptive evolution. This book satisfies the need for a truly general book on development, plasticity and evolution that applies to living organisms in all of their life stages and environments. Using an immense compendium of examples on many kinds of organisms, from viruses and bacteria to higher plants and animals, it shows how the phenotype is reorganized during evolution to produce novelties, and how alternative phenotypes occupy a pivotal role as a phase of evolution that fosters diversification and speeds change. The arguments of this book call for a new view of the major themes of evolutionary biology, as shown in chapters on gradualism, homology, environmental induction, speciation, radiation, macroevolution, punctuation, and the maintenance of sex. No other treatment of development and evolution since Darwin's offers such a comprehensive and critical discussion of the relevant issues. Developmental Plasticity and Evolution is designed for biologists interested in the development and evolution of behavior, life-history patterns, ecology, physiology, morphology and speciation. It will also appeal to evolutionary paleontologists, anthropologists, psychologists, and teachers of general biology.

scholarly journals Adenovirus E1A specifically blocks SWI/SNF-dependent transcriptional activation.

1996 ◽  
Vol 16 (10) ◽  
pp. 5737-5743 ◽  
Author(s):  
M E Miller ◽  
B R Cairns ◽  
R S Levinson ◽  
K R Yamamoto ◽  
D A Engel ◽  
...  
Keyword(s):  
Transcriptional Activation ◽  
Cellular Transformation ◽  
Transcriptional Coactivator ◽  
Gene Encoding ◽  
Adenovirus E1a ◽  
Transcriptional Regulatory ◽  
Genes Encoding ◽  
Regulatory Complex ◽  
Activation Pathways ◽  
Coactivator P300

Expression of the adenovirus E1A243 oncoprotein in Saccharomyces cerevisiae produces a slow-growth phenotype with accumulation of cells in the G1 phase of the cell cycle. This effect is due to the N-terminal and CR1 domains of E1A243, which in rodent cells are involved in triggering cellular transformation and also in binding to the cellular transcriptional coactivator p300. A genetic screen was undertaken to identify genes required for the function of E1A243 in S. cerevisiae. This screen identified SNF12, a gene encoding the 73-kDa subunit of the SWI/SNF transcriptional regulatory complex. Mutation of genes encoding known members of the SWI/SNF complex also led to loss of E1A function, suggesting that the SWI/SNF complex is a target of E1A243. Moreover, expression of E1A in wild-type cells specifically blocked transcriptional activation of the INO1 and SUC2 genes, whose activation pathways are distinct but have a common requirement for the SWI/SNF complex. These data demonstrate a specific functional interaction between E1A and the SWI/SNF complex and suggest that a similar interaction takes place in rodent and human cells.

HDAC1-Smad3-mSin3Acomplex is required for Smad3-induced transcriptional inhibition of hepatocyte growth factor receptor in human lung cancers

2020 ◽  
Author(s):  
Hao-Xin Gui ◽  
Jun Peng ◽  
Ze-Ping Yang ◽  
Lu-Yao Chen ◽  
Hong Zeng ◽  
...  
Keyword(s):  
Transcriptional Activation ◽  
Molecular Mechanisms ◽  
Growth Factor Receptor ◽  
Mrna Levels ◽  
Lung Cancers ◽  
Transcriptional Inhibition ◽  
Transcriptional Suppression ◽  
Transcriptional Regulatory ◽  
Regulatory Complex ◽  
Cancer Tissues

Abstract c-Met hyperactivity has been observed in numerous neoplasms. Several researchers have shown that the abnormal activation of c-Met is mainly caused by transcriptional activation. However, the molecular mechanism behind this transcriptional regulation is poorly understood. Here, we suggest that Smad3 negatively regulates the expression and activation of c-Met via a transcriptional mechanism. We explore the molecular mechanisms that underlie Smad3-induced c-Met transcription inhibition. We found in contrast to the high expression of c-Met, Smad3 showed low protein and mRNA levels. Smad3 and c-Met expression was inconsistent between lung cancer tissues and cell lines. We also found that Smad3 overexpression suppresses whereas Smad3 knockdown significantly promotes EMT and production of the angiogenic factors VEGF, CTGF and COX-2 through the ERK1/2 pathway. In addition, Smad3 overexpression decreases whereas Smad3 knockdown significantly increases protein and mRNA levels of invasion related β-catenin and FAK through the PI3K/Akt pathway. Furthermore, using the ChIP analysis method, we demonstrate that a transcriptional regulatory complex consisting of HDAC1, Smad3 and mSin3A binds to the promoter of the c-Met gene. By either silencing endogenous mSin3A expression with siRNA or by pretreating cells with a specific HDAC1 inhibitor (MS-275), Smad3-induced transcriptional suppression of c-Met could be effectively attenuated. These results demonstrate that Smad3-induced inhibition of c-Met transcription depends on of a functional transcriptional regulatory complex that includes Smad3, mSin3A and HDAC1 at the c-Met promoter. Collectively, our findings reveal a new regulatory mechanism of c-Met signaling, and suggest a potential molecular target for the development of anticancer drugs.

scholarly journals Combined Analysis of MicroRNAs and Target Genes Revealed miR156-SPLs and miR172-AP2 Are Involved in a Delayed Flowering Phenomenon After Chromosome Doubling in Black Goji (Lycium ruthencium)

2021 ◽  
Vol 12 ◽  
Author(s):  
Shupei Rao ◽  
Yue Li ◽  
Jinhuan Chen
Keyword(s):  
Flowering Time ◽  
Messenger Rna ◽  
Target Genes ◽  
Higher Plants ◽  
Chromosome Doubling ◽  
Late Flowering ◽  
New Perspective ◽  
Commercial Applications ◽  
Flowering Regulation ◽  
Delayed Flowering

Polyploidy, which is widely distributed in angiosperms, presents extremely valuable commercial applications in plant growth and reproduction. The flower development process of higher plants is essential for genetic improvement. Nevertheless, the reproduction difference between polyploidy and the polyploid florescence regulatory network from the perspective of microRNA (miRNA) remains to be elucidated. In this study, the autotetraploid of Lycium ruthenicum showed late-flowering traits compared with the progenitor. Combining the association of miRNA and next-generation transcriptome technology, the late-flowering characteristics triggered by chromosome duplication may be caused by the age pathway involved in miR156-SPLs and miR172-AP2, which inhibits the messenger RNA (mRNA) transcripts of FT in the leaves. Subsequently, FT was transferred to the shoot apical meristem (SAM) to inhibit the expression of the flowering integration factor SOC1, which can eventually result in delayed flowering time. Our exploration of the flowering regulation network and the control of the flowering time are vital to the goji producing in the late frost area, which provides a new perspective for exploring the intrinsic molecular mechanism of polyploid and the reproductive development of flowering plants.

scholarly journals Rap1p Requires Gcr1p and Gcr2p Homodimers to Activate Ribosomal Protein and Glycolytic Genes, Respectively

Genetics ◽  
2001 ◽  
Vol 158 (1) ◽  
pp. 133-143 ◽  
Author(s):  
Stephen J Deminoff ◽  
George M Santangelo
Keyword(s):  
Ribosomal Protein ◽  
Transcriptional Activation ◽  
Leucine Zipper ◽  
Point Mutations ◽  
Growth Defect ◽  
Phosphorylation State ◽  
Glycolytic Gene ◽  
Activation Mechanisms ◽  
Regulatory Complex ◽  
Activator Complex

Abstract Efficient transcription of ribosomal protein (RP) and glycolytic genes requires the Rap1p/Gcr1p regulatory complex. A third factor, Gcr2p, is required for only the glycolytic (specialized) mode of transcriptional activation. It is recruited to the complex by Gcr1p and likely mediates a change in the phosphorylation state and/or conformation of the latter. We show here that leucine zipper motifs in Gcr1p and Gcr2p (1LZ and 2LZ) are each specific to one of the two activation mechanisms—mutations in 1LZ and 2LZ impair transcription of RP and glycolytic genes, respectively. Although neither class of mutations causes more than a mild growth defect, simultaneous impairment of 1LZ and 2LZ results in a severe synthetic defect and a reduction in the expression of both sets of genes. Intracistronic complementation by point mutations in the charged e and g positions confirmed that Gcr1p/Gcr1p and Gcr2p/Gcr2p homodimers are the forms required for the different roles of the activator complex. Direct heterodimerization between 1LZ and 2LZ apparently does not occur. Dichotomous Rap1p activation and its striking requirement for distinct homodimeric subunits give cells the capacity to switch between coordinated and uncoupled RP and glycolytic gene regulation.

scholarly journals DNA Recognition by the Herpes Simplex Virus Transactivator VP16: a Novel DNA-Binding Structure

2001 ◽  
Vol 21 (14) ◽  
pp. 4700-4712 ◽  
Author(s):  
Robert Babb ◽  
C. Chris Huang ◽  
Deborah J. Aufiero ◽  
Winship Herr
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Dna Binding ◽  
Transcriptional Activation ◽  
Binding Activity ◽  
Dna Binding Activity ◽  
Transcriptional Regulatory ◽  
Regulatory Complex ◽  
Simplex Virus ◽  
Carboxy Terminal

ABSTRACT Upon infection, the herpes simplex virus (HSV) transcriptional activator VP16 directs the formation of a multiprotein-DNA complex—the VP16-induced complex—with two cellular proteins, the host cell factor HCF-1 and the POU domain transcription factor Oct-1, on TAATGARAT-containing sequences found in the promoters of HSV immediate-early genes. HSV VP16 contains carboxy-terminal sequences important for transcriptional activation and a central conserved core that is important for VP16-induced complex assembly. On its own, VP16 displays little, if any, sequence-specific DNA-binding activity. We show here that, within the VP16-induced complex, however, the VP16 core has an important role in DNA binding. Mutation of basic residues on the surface of the VP16 core reveals a novel DNA-binding surface with essential residues which are conserved among VP16 orthologs. These results illuminate how, through association with DNA, VP16 is able to interpret cis-regulatory signals in the DNA to direct the assembly of a multiprotein-DNA transcriptional regulatory complex.

scholarly journals Frequent fires prime plant developmental responses to burning

2019 ◽  
Vol 286 (1909) ◽  
pp. 20191315 ◽  
Author(s):  
Kimberley J. Simpson ◽  
Jill K. Olofsson ◽  
Brad S. Ripley ◽  
Colin P. Osborne
Keyword(s):  
Developmental Plasticity ◽  
Fire Regime ◽  
Fire Regimes ◽  
Fire Frequency ◽  
Fire Exposure ◽  
Regime Changes ◽  
Below Ground ◽  
Developmental Responses ◽  
In Fire ◽  
Plastic Responses

Coping with temporal variation in fire requires plants to have plasticity in traits that promote persistence, but how plastic responses to current conditions are affected by past fire exposure remains unknown. We investigate phenotypic divergence between populations of four resprouting grasses exposed to differing experimental fire regimes (annually burnt or unburnt for greater than 35 years) and test whether divergence persists after plants are grown in a common environment for 1 year. Traits relating to flowering and biomass allocation were measured before plants were experimentally burnt, and their regrowth was tracked. Genetic differentiation between populations was investigated for a subset of individuals. Historic fire frequency influenced traits relating to flowering and below-ground investment. Previously burnt plants produced more inflorescences and invested proportionally more biomass below ground, suggesting a greater capacity for recruitment and resprouting than unburnt individuals. Tiller-scale regrowth rate did not differ between treatments, but prior fire exposure enhanced total regrown biomass in two species. We found no consistent genetic differences between populations suggesting trait differences arose from developmental plasticity. Grass development is influenced by prior fire exposure, independent of current environmental conditions. This priming response to fire, resulting in adaptive trait changes, may produce communities more resistant to future fire regime changes.

TCP transcription factors: architectures of plant form

2013 ◽  
Vol 4 (2) ◽  
pp. 111-127 ◽  
Author(s):  
Nora G. Uberti Manassero ◽  
Ivana L. Viola ◽  
Elina Welchen ◽  
Daniel H. Gonzalez
Keyword(s):  
Transcription Factors ◽  
Plant Development ◽  
Current Knowledge ◽  
Hormone Responses ◽  
Plant Form ◽  
Developmental Responses ◽  
Available Information ◽  
Dna Complex ◽  
Shed Light

AbstractAfter its initial definition in 1999, the TCP family of transcription factors has become the focus of a multiplicity of studies related with plant development at the cellular, organ, and tissue levels. Evidence has accumulated indicating that TCP transcription factors are the main regulators of plant form and architecture and constitute a tool through which evolution shapes plant diversity. The TCP transcription factors act in a multiplicity of pathways related with cell proliferation and hormone responses. In recent years, the molecular pathways of TCP protein action and biochemical studies on their mode of interaction with DNA have begun to shed light on their mechanism of action. However, the available information is fragmented and a unifying view of TCP protein action is lacking, as well as detailed structural studies of the TCP-DNA complex. Also important, the possible role of TCP proteins as integrators of plant developmental responses to the environment has deserved little attention. In this review, we summarize the current knowledge about the structure and functions of TCP transcription factors and analyze future perspectives for the study of the role of these proteins and their use to modify plant development.

scholarly journals Functional and mechanistic studies of XPC DNA-repair complex as transcriptional coactivator in embryonic stem cells

2015 ◽  
Vol 112 (18) ◽  
pp. E2317-E2326 ◽  
Author(s):  
Claudia Cattoglio ◽  
Elisa T. Zhang ◽  
Ivan Grubisic ◽  
Kunitoshi Chiba ◽  
Yick W. Fong ◽  
...  
Keyword(s):  
Stem Cells ◽  
Dna Repair ◽  
Stem Cell ◽  
Transcriptional Activation ◽  
Embryonic Stem ◽  
Chromatin Regulators ◽  
Regulatory Circuits ◽  
Functional Aspects ◽  
Regulatory Complex ◽  
Induced Pluripotent

The embryonic stem cell (ESC) state is transcriptionally controlled by OCT4, SOX2, and NANOG with cofactors, chromatin regulators, noncoding RNAs, and other effectors of signaling pathways. Uncovering components of these regulatory circuits and their interplay provides the knowledge base to deploy ESCs and induced pluripotent stem cells. We recently identified the DNA-repair complex xeroderma pigmentosum C (XPC)-RAD23B-CETN2 as a stem cell coactivator (SCC) required for OCT4/SOX2 transcriptional activation. Here we investigate the role of SCC genome-wide in murine ESCs by mapping regions bound by RAD23B and analyzing transcriptional profiles of SCC-depleted ESCs. We establish OCT4 and SOX2 as the primary transcription factors recruiting SCC to regulatory regions of pluripotency genes and identify the XPC subunit as essential for interaction with the two proteins. The present study reveals new mechanistic and functional aspects of SCC transcriptional activity, and thus underscores the diversified functions of this regulatory complex.

scholarly journals Controlling Apomixis: Shared Features and Distinct Characteristics of Gene Regulation

Genes ◽  
2020 ◽  
Vol 11 (3) ◽  
pp. 329 ◽  
Author(s):  
Anja Schmidt
Keyword(s):  
Transcriptional Activation ◽  
Genetic Basis ◽  
Molecular Mechanisms ◽  
Rna Binding ◽  
Rna Binding Proteins ◽  
Higher Plants ◽  
Rna Helicases ◽  
Seed Formation ◽  
Molecular Control ◽  
Sexual And Asexual Reproduction

In higher plants, sexual and asexual reproduction through seeds (apomixis) have evolved as alternative strategies. As apomixis leads to the formation of clonal offspring, its great potential for agricultural applications has long been recognized. However, the genetic basis and the molecular control underlying apomixis and its evolutionary origin are to date not fully understood. Both in sexual and apomictic plants, reproduction is tightly controlled by versatile mechanisms regulating gene expression, translation, and protein abundance and activity. Increasing evidence suggests that interrelated pathways including epigenetic regulation, cell-cycle control, hormonal pathways, and signal transduction processes are relevant for apomixis. Additional molecular mechanisms are being identified that involve the activity of DNA- and RNA-binding proteins, such as RNA helicases which are increasingly recognized as important regulators of reproduction. Together with other factors including non-coding RNAs, their association with ribosomes is likely to be relevant for the formation and specification of the apomictic reproductive lineage. Subsequent seed formation appears to involve an interplay of transcriptional activation and repression of developmental programs by epigenetic regulatory mechanisms. In this review, insights into the genetic basis and molecular control of apomixis are presented, also taking into account potential relations to environmental stress, and considering aspects of evolution.

Sign in / Sign up

Export Citation Format

Share Document