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1.
Sci Adv ; 10(6): eadi2671, 2024 Feb 09.
Artigo em Inglês | MEDLINE | ID: mdl-38335286

RESUMO

The adult intestine is a regionalized organ, whose size and cellular composition are adjusted in response to nutrient status. This involves dynamic regulation of intestinal stem cell (ISC) proliferation and differentiation. How nutrient signaling controls cell fate decisions to drive regional changes in cell-type composition remains unclear. Here, we show that intestinal nutrient adaptation involves region-specific control of cell size, cell number, and differentiation. We uncovered that activation of mTOR complex 1 (mTORC1) increases ISC size in a region-specific manner. mTORC1 activity promotes Delta expression to direct cell fate toward the absorptive enteroblast lineage while inhibiting secretory enteroendocrine cell differentiation. In aged flies, the ISC mTORC1 signaling is deregulated, being constitutively high and unresponsive to diet, which can be mitigated through lifelong intermittent fasting. In conclusion, mTORC1 signaling contributes to the ISC fate decision, enabling regional control of intestinal cell differentiation in response to nutrition.


Assuntos
Mucosa Intestinal , Intestinos , Diferenciação Celular , Linhagem da Célula , Proliferação de Células , Mucosa Intestinal/metabolismo , Alvo Mecanístico do Complexo 1 de Rapamicina/metabolismo , Nutrientes , Células-Tronco/metabolismo , Serina-Treonina Quinases TOR/metabolismo , Drosophila
2.
Elife ; 102021 03 16.
Artigo em Inglês | MEDLINE | ID: mdl-33724181

RESUMO

Tissue homeostasis requires long-term lineage fidelity of somatic stem cells. Whether and how age-related changes in somatic stem cells impact the faithful execution of lineage decisions remains largely unknown. Here, we address this question using genome-wide chromatin accessibility and transcriptome analysis as well as single-cell RNA-seq to explore stem-cell-intrinsic changes in the aging Drosophila intestine. These studies indicate that in stem cells of old flies, promoters of Polycomb (Pc) target genes become differentially accessible, resulting in the increased expression of enteroendocrine (EE) cell specification genes. Consistently, we find age-related changes in the composition of the EE progenitor cell population in aging intestines, as well as a significant increase in the proportion of EE-specified intestinal stem cells (ISCs) and progenitors in aging flies. We further confirm that Pc-mediated chromatin regulation is a critical determinant of EE cell specification in the Drosophila intestine. Pc is required to maintain expression of stem cell genes while ensuring repression of differentiation and specification genes. Our results identify Pc group proteins as central regulators of lineage identity in the intestinal epithelium and highlight the impact of age-related decline in chromatin regulation on tissue homeostasis.


Assuntos
Células-Tronco Adultas/metabolismo , Linhagem da Célula/genética , Proteínas de Drosophila/genética , Intestinos/citologia , Proteínas do Grupo Polycomb/genética , Envelhecimento/genética , Animais , Diferenciação Celular/genética , Cromatina/genética , Cromatina/metabolismo , Drosophila/genética , Proteínas de Drosophila/metabolismo , Enterócitos/metabolismo , Células Enteroendócrinas/metabolismo , Regulação da Expressão Gênica , Homeostase , Mucosa Intestinal/metabolismo , Proteínas do Grupo Polycomb/metabolismo , Transcriptoma
3.
Nat Commun ; 11(1): 3932, 2020 08 04.
Artigo em Inglês | MEDLINE | ID: mdl-32753580

RESUMO

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

4.
Nat Commun ; 11(1): 2493, 2020 05 19.
Artigo em Inglês | MEDLINE | ID: mdl-32427826

RESUMO

Genetic changes acquired during in vitro culture pose a risk for the successful application of stem cells in regenerative medicine. To assess the genetic risks induced by culturing, we determined all mutations in individual human stem cells by whole genome sequencing. Individual pluripotent, intestinal, and liver stem cells accumulate 3.5 ± 0.5, 7.2 ± 1.1 and 8.3 ± 3.6 base substitutions per population doubling, respectively. The annual in vitro mutation accumulation rate of adult stem cells is nearly 40-fold higher than the in vivo mutation accumulation rate. Mutational signature analysis reveals that in vitro induced mutations are caused by oxidative stress. Reducing oxygen tension in culture lowers the mutational load. We use the mutation rates, spectra, and genomic distribution to model the accumulation of oncogenic mutations during typical in vitro expansion, manipulation or screening experiments using human stem cells. Our study provides empirically defined parameters to assess the mutational risk of stem cell based therapies.


Assuntos
Células-Tronco Adultas/metabolismo , Análise Mutacional de DNA/métodos , Células-Tronco Pluripotentes Induzidas/metabolismo , Mutação , Adulto , Células-Tronco Adultas/citologia , Algoritmos , Células Cultivadas , Humanos , Células-Tronco Pluripotentes Induzidas/citologia , Intestinos/citologia , Fígado/citologia , Fígado/metabolismo , Modelos Genéticos , Acúmulo de Mutações , Taxa de Mutação , Medicina Regenerativa/métodos , Sequenciamento Completo do Genoma/métodos
5.
Genome Med ; 11(1): 79, 2019 12 04.
Artigo em Inglês | MEDLINE | ID: mdl-31801603

RESUMO

BACKGROUND: Genomic structural variants (SVs) can affect many genes and regulatory elements. Therefore, the molecular mechanisms driving the phenotypes of patients carrying de novo SVs are frequently unknown. METHODS: We applied a combination of systematic experimental and bioinformatic methods to improve the molecular diagnosis of 39 patients with multiple congenital abnormalities and/or intellectual disability harboring apparent de novo SVs, most with an inconclusive diagnosis after regular genetic testing. RESULTS: In 7 of these cases (18%), whole-genome sequencing analysis revealed disease-relevant complexities of the SVs missed in routine microarray-based analyses. We developed a computational tool to predict the effects on genes directly affected by SVs and on genes indirectly affected likely due to the changes in chromatin organization and impact on regulatory mechanisms. By combining these functional predictions with extensive phenotype information, candidate driver genes were identified in 16/39 (41%) patients. In 8 cases, evidence was found for the involvement of multiple candidate drivers contributing to different parts of the phenotypes. Subsequently, we applied this computational method to two cohorts containing a total of 379 patients with previously detected and classified de novo SVs and identified candidate driver genes in 189 cases (50%), including 40 cases whose SVs were previously not classified as pathogenic. Pathogenic position effects were predicted in 28% of all studied cases with balanced SVs and in 11% of the cases with copy number variants. CONCLUSIONS: These results demonstrate an integrated computational and experimental approach to predict driver genes based on analyses of WGS data with phenotype association and chromatin organization datasets. These analyses nominate new pathogenic loci and have strong potential to improve the molecular diagnosis of patients with de novo SVs.


Assuntos
Estudos de Associação Genética , Doenças Genéticas Inatas/diagnóstico , Doenças Genéticas Inatas/genética , Predisposição Genética para Doença , Variação Genética , Fenótipo , Biologia Computacional/métodos , Variações do Número de Cópias de DNA , Genoma Humano , Variação Estrutural do Genoma , Humanos , Anotação de Sequência Molecular , Sequenciamento Completo do Genoma
6.
Nat Commun ; 10(1): 4123, 2019 09 11.
Artigo em Inglês | MEDLINE | ID: mdl-31511511

RESUMO

In adult epithelial stem cell lineages, the precise differentiation of daughter cells is critical to maintain tissue homeostasis. Notch signaling controls the choice between absorptive and entero-endocrine cell differentiation in both the mammalian small intestine and the Drosophila midgut, yet how Notch promotes lineage restriction remains unclear. Here, we describe a role for the transcription factor Klumpfuss (Klu) in restricting the fate of enteroblasts (EBs) in the Drosophila intestine. Klu is induced in Notch-positive EBs and its activity restricts cell fate towards the enterocyte (EC) lineage. Transcriptomics and DamID profiling show that Klu suppresses enteroendocrine (EE) fate by repressing the action of the proneural gene Scute, which is essential for EE differentiation. Loss of Klu results in differentiation of EBs into EE cells. Our findings provide mechanistic insight into how lineage commitment in progenitor cell differentiation can be ensured downstream of initial specification cues.


Assuntos
Linhagem da Célula , Proteínas de Ligação a DNA/metabolismo , Proteínas de Drosophila/metabolismo , Drosophila melanogaster/citologia , Enterócitos/citologia , Intestinos/citologia , Células-Tronco/citologia , Fatores de Transcrição/metabolismo , Animais , Carcinogênese/metabolismo , Carcinogênese/patologia , Diferenciação Celular , Proliferação de Células , Modelos Biológicos , Ligação Proteica , Receptores Notch/metabolismo , Transdução de Sinais , Células-Tronco/metabolismo
7.
Nat Commun ; 8(1): 1326, 2017 11 06.
Artigo em Inglês | MEDLINE | ID: mdl-29109544

RESUMO

Despite improvements in genomics technology, the detection of structural variants (SVs) from short-read sequencing still poses challenges, particularly for complex variation. Here we analyse the genomes of two patients with congenital abnormalities using the MinION nanopore sequencer and a novel computational pipeline-NanoSV. We demonstrate that nanopore long reads are superior to short reads with regard to detection of de novo chromothripsis rearrangements. The long reads also enable efficient phasing of genetic variations, which we leveraged to determine the parental origin of all de novo chromothripsis breakpoints and to resolve the structure of these complex rearrangements. Additionally, genome-wide surveillance of inherited SVs reveals novel variants, missed in short-read data sets, a large proportion of which are retrotransposon insertions. We provide a first exploration of patient genome sequencing with a nanopore sequencer and demonstrate the value of long-read sequencing in mapping and phasing of SVs for both clinical and research applications.


Assuntos
Mapeamento Cromossômico/métodos , Cromotripsia , Análise Mutacional de DNA/métodos , Nanoporos , Anormalidades Múltiplas/genética , Algoritmos , Mapeamento Cromossômico/estatística & dados numéricos , Biologia Computacional , Análise Mutacional de DNA/estatística & dados numéricos , Rearranjo Gênico , Variação Genética , Sequenciamento de Nucleotídeos em Larga Escala/métodos , Sequenciamento de Nucleotídeos em Larga Escala/estatística & dados numéricos , Humanos
8.
Cell Rep ; 12(2): 346-58, 2015 Jul 14.
Artigo em Inglês | MEDLINE | ID: mdl-26146076

RESUMO

Deciphering contributions of specific cell types to organ function is experimentally challenging. The Drosophila midgut is a dynamic organ with five morphologically and functionally distinct regions (R1-R5), each composed of multipotent intestinal stem cells (ISCs), progenitor enteroblasts (EBs), enteroendocrine cells (EEs), enterocytes (ECs), and visceral muscle (VM). To characterize cellular specialization and regional function in this organ, we generated RNA-sequencing transcriptomes of all five cell types isolated by FACS from each of the five regions, R1-R5. In doing so, we identify transcriptional diversities among cell types and document regional differences within each cell type that define further specialization. We validate cell-specific and regional Gal4 drivers; demonstrate roles for transporter Smvt and transcription factors GATAe, Sna, and Ptx1 in global and regional ISC regulation, and study the transcriptional response of midgut cells upon infection. The resulting transcriptome database (http://flygutseq.buchonlab.com) will foster studies of regionalization, homeostasis, immunity, and cell-cell interactions.


Assuntos
Drosophila/metabolismo , Intestinos/citologia , Transcriptoma , Músculos Abdominais/citologia , Músculos Abdominais/metabolismo , Animais , Diferenciação Celular , Proliferação de Células , Sobrevivência Celular , Drosophila/genética , Proteínas de Drosophila/antagonistas & inibidores , Proteínas de Drosophila/genética , Proteínas de Drosophila/metabolismo , Enterócitos/citologia , Enterócitos/metabolismo , Células Enteroendócrinas/citologia , Células Enteroendócrinas/metabolismo , Fatores de Transcrição GATA/antagonistas & inibidores , Fatores de Transcrição GATA/genética , Fatores de Transcrição GATA/metabolismo , Mucosa Intestinal/metabolismo , Análise de Componente Principal , Interferência de RNA , RNA Interferente Pequeno/metabolismo , Fatores de Transcrição da Família Snail , Células-Tronco/citologia , Células-Tronco/metabolismo , Simportadores/metabolismo , Fatores de Transcrição/metabolismo
9.
EMBO J ; 33(24): 2967-82, 2014 Dec 17.
Artigo em Inglês | MEDLINE | ID: mdl-25298397

RESUMO

Snail family transcription factors are expressed in various stem cell types, but their function in maintaining stem cell identity is unclear. In the adult Drosophila midgut, the Snail homolog Esg is expressed in intestinal stem cells (ISCs) and their transient undifferentiated daughters, termed enteroblasts (EB). We demonstrate here that loss of esg in these progenitor cells causes their rapid differentiation into enterocytes (EC) or entero-endocrine cells (EE). Conversely, forced expression of Esg in intestinal progenitor cells blocks differentiation, locking ISCs in a stem cell state. Cell type-specific transcriptome analysis combined with Dam-ID binding studies identified Esg as a major repressor of differentiation genes in stem and progenitor cells. One critical target of Esg was found to be the POU-domain transcription factor, Pdm1, which is normally expressed specifically in differentiated ECs. Ectopic expression of Pdm1 in progenitor cells was sufficient to drive their differentiation into ECs. Hence, Esg is a critical stem cell determinant that maintains stemness by repressing differentiation-promoting factors, such as Pdm1.


Assuntos
Diferenciação Celular , Proteínas de Drosophila/metabolismo , Drosophila/fisiologia , Células-Tronco/efeitos dos fármacos , Células-Tronco/fisiologia , Animais , Trato Gastrointestinal/fisiologia , Deleção de Genes , Expressão Gênica , Perfilação da Expressão Gênica
10.
Cell Rep ; 7(2): 588-598, 2014 Apr 24.
Artigo em Inglês | MEDLINE | ID: mdl-24726363

RESUMO

One promising approach for in vivo studies of cell proliferation is the FUCCI system (fluorescent ubiquitination-based cell cycle indicator). Here, we report the development of a Drosophila-specific FUCCI system (Fly-FUCCI) that allows one to distinguish G1, S, and G2 phases of interphase. Fly-FUCCI relies on fluorochrome-tagged degrons from the Cyclin B and E2F1 proteins, which are degraded by the ubiquitin E3-ligases APC/C and CRL4(Cdt2), during mitosis or the onset of S phase, respectively. These probes can track cell-cycle patterns in cultured Drosophila cells, eye and wing imaginal discs, salivary glands, the adult midgut, and probably other tissues. To support a broad range of experimental applications, we have generated a toolkit of transgenic Drosophila lines that express the Fly-FUCCI probes under control of the UASt, UASp, QUAS, and ubiquitin promoters. The Fly-FUCCI system should be a valuable tool for visualizing cell-cycle activity during development, tissue homeostasis, and neoplastic growth.


Assuntos
Ciclo Celular , Proliferação de Células , Drosophila/citologia , Microscopia de Fluorescência/métodos , Ubiquitinação , Ciclossomo-Complexo Promotor de Anáfase/genética , Ciclossomo-Complexo Promotor de Anáfase/metabolismo , Animais , Linhagem Celular , Ciclina B/genética , Ciclina B/metabolismo , Drosophila/genética , Drosophila/metabolismo , Fator de Transcrição E2F1/genética , Fator de Transcrição E2F1/metabolismo , Especificidade de Órgãos
11.
PLoS Genet ; 7(11): e1002362, 2011 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-22102824

RESUMO

Cell proliferation and differentiation are regulated in a highly coordinated and inverse manner during development and tissue homeostasis. Terminal differentiation usually coincides with cell cycle exit and is thought to engage stable transcriptional repression of cell cycle genes. Here, we examine the robustness of the post-mitotic state, using Caenorhabditis elegans muscle cells as a model. We found that expression of a G1 Cyclin and CDK initiates cell cycle re-entry in muscle cells without interfering with the differentiated state. Cyclin D/CDK4 (CYD-1/CDK-4) expression was sufficient to induce DNA synthesis in muscle cells, in contrast to Cyclin E/CDK2 (CYE-1/CDK-2), which triggered mitotic events. Tissue-specific gene-expression profiling and single molecule FISH experiments revealed that Cyclin D and E kinases activate an extensive and overlapping set of cell cycle genes in muscle, yet failed to induce some key activators of G1/S progression. Surprisingly, CYD-1/CDK-4 also induced an additional set of genes primarily associated with growth and metabolism, which were not activated by CYE-1/CDK-2. Moreover, CYD-1/CDK-4 expression also down-regulated a large number of genes enriched for catabolic functions. These results highlight distinct functions for the two G1 Cyclin/CDK complexes and reveal a previously unknown activity of Cyclin D/CDK-4 in regulating metabolic gene expression. Furthermore, our data demonstrate that many cell cycle genes can still be transcriptionally induced in post-mitotic muscle cells, while maintenance of the post-mitotic state might depend on stable repression of a limited number of critical cell cycle regulators.


Assuntos
Caenorhabditis elegans/genética , Ciclo Celular/genética , Ciclina D/genética , Ciclina D/metabolismo , Ciclina E/genética , Quinase 2 Dependente de Ciclina/genética , Quinase 4 Dependente de Ciclina/genética , Células Musculares/citologia , Animais , Animais Geneticamente Modificados , Caenorhabditis elegans/metabolismo , Diferenciação Celular , Proliferação de Células , Ciclina E/metabolismo , Quinase 2 Dependente de Ciclina/metabolismo , Quinase 4 Dependente de Ciclina/metabolismo , Replicação do DNA/genética , Regulação da Expressão Gênica no Desenvolvimento , Células Musculares/metabolismo , Especificidade de Órgãos/genética
12.
Dev Biol ; 350(2): 358-69, 2011 Feb 15.
Artigo em Inglês | MEDLINE | ID: mdl-21146520

RESUMO

DNA replication and its connection to M phase restraint are studied extensively at the level of single cells but rarely in the context of a developing animal. C. elegans lin-6 mutants lack DNA synthesis in postembryonic somatic cell lineages, while entry into mitosis continues. These mutants grow slowly and either die during larval development or develop into sterile adults. We found that lin-6 corresponds to mcm-4 and encodes an evolutionarily conserved component of the MCM2-7 pre-RC and replicative helicase complex. The MCM-4 protein is expressed in all dividing cells during embryonic and postembryonic development and associates with chromatin in late anaphase. Induction of cell cycle entry and differentiation continues in developing mcm-4 larvae, even in cells that went through abortive division. In contrast to somatic cells in mcm-4 mutants, the gonad continues DNA replication and cell division until late larval development. Expression of MCM-4 in the epidermis (also known as hypodermis) is sufficient to rescue the growth retardation and lethality of mcm-4 mutants. While the somatic gonad and germline show substantial ability to cope with lack of zygotic mcm-4 function, mcm-4 is specifically required in the epidermis for growth and survival of the whole organism. Thus, C. elegans mcm-4 has conserved functions in DNA replication and replication checkpoint control but also shows unexpected tissue-specific requirements.


Assuntos
Proteínas de Caenorhabditis elegans/fisiologia , Caenorhabditis elegans/crescimento & desenvolvimento , Proteínas de Ciclo Celular/fisiologia , Ciclo Celular , Replicação do DNA , Epiderme/fisiologia , Animais , Caenorhabditis elegans/citologia , Caenorhabditis elegans/metabolismo , Diferenciação Celular , Divisão Celular , Sobrevivência Celular , Fase G1 , Mitose , Especificidade de Órgãos , Fase S
13.
Curr Biol ; 17(16): R630-2, 2007 Aug 21.
Artigo em Inglês | MEDLINE | ID: mdl-17714648

RESUMO

All eukaryotes use multiple controls to restrict DNA replication to once per cell cycle. Nevertheless, inactivation of a single gene, cul-4, causes massive re-replication in Caenorhabditis elegans. A novel study explains this dramatic phenotype by demonstrating that the CUL-4 E3 ligase simultaneously controls two critical licensing factors: CDT-1 and CDC-6.


Assuntos
Caenorhabditis elegans/genética , Replicação do DNA , Animais , Caenorhabditis elegans/citologia , Caenorhabditis elegans/metabolismo , Proteínas de Caenorhabditis elegans/metabolismo , Ciclo Celular , Proteínas de Ciclo Celular/metabolismo , Genoma Helmíntico , Ligases/metabolismo
14.
Plant Physiol ; 142(1): 352-63, 2006 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-16829584

RESUMO

Caterpillars of the herbivore Pieris rapae stimulate the production of jasmonic acid (JA) and ethylene (ET) in Arabidopsis (Arabidopsis thaliana) and trigger a defense response that affects insect performance on systemic tissues. To investigate the spectrum of effectiveness of P. rapae-induced resistance, we examined the level of resistance against different pathogens. Although the necrotrophic fungus Alternaria brassicicola is sensitive to JA-dependent defenses, herbivore-induced resistance was not effective against this pathogen. By contrast, caterpillar feeding significantly reduced disease caused by the bacterial pathogens Pseudomonas syringae pv tomato and Xanthomonas campestris pv armoraciae. However, this effect was apparent only locally in caterpillar-damaged tissue. Arabidopsis mutants jar1, coi1, ein2, sid2, eds5, and npr1 showed wild-type levels of P. rapae-induced protection against P. syringae pv tomato, suggesting that this local, herbivore-induced defense response does not depend exclusively on either JA, ET, or salicylic acid (SA). Resistance against the biotroph Turnip crinkle virus (TCV) requires SA, but not JA and ET. Nevertheless, herbivore feeding strongly affected TCV multiplication and TCV lesion formation, also in systemic tissues. Wounding alone was not effective, but application of P. rapae regurgitate onto the wounds induced a similar level of protection. Analysis of SA-induced PATHOGENESIS RELATED-1 (PR-1) expression revealed that P. rapae grazing primed Arabidopsis leaves for augmented expression of SA-dependent defenses. Pharmacological experiments showed that ET acts synergistically on SA-induced PR-1, suggesting that the increased production of ET upon herbivore feeding sensitizes the tissue to respond faster to SA, thereby contributing to an enhanced defensive capacity toward pathogens, such as TCV, that trigger SA-dependent defenses upon infection.


Assuntos
Arabidopsis/microbiologia , Borboletas/fisiologia , Larva/fisiologia , Alternaria/fisiologia , Animais , Arabidopsis/fisiologia , Arabidopsis/virologia , Comportamento Alimentar , Doenças das Plantas , Folhas de Planta/microbiologia , Vírus de Plantas/fisiologia , Pseudomonas syringae/fisiologia , Ácido Salicílico/metabolismo , Xanthomonas campestris/fisiologia
15.
Plant Cell ; 15(3): 760-70, 2003 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-12615947

RESUMO

Plant defenses against pathogens and insects are regulated differentially by cross-communicating signal transduction pathways in which salicylic acid (SA) and jasmonic acid (JA) play key roles. In this study, we investigated the molecular mechanism of the antagonistic effect of SA on JA signaling. Arabidopsis plants unable to accumulate SA produced 25-fold higher levels of JA and showed enhanced expression of the JA-responsive genes LOX2, PDF1.2, and VSP in response to infection by Pseudomonas syringae pv tomato DC3000, indicating that in wild-type plants, pathogen-induced SA accumulation is associated with the suppression of JA signaling. Analysis of the Arabidopsis mutant npr1, which is impaired in SA signal transduction, revealed that the antagonistic effect of SA on JA signaling requires the regulatory protein NPR1. Nuclear localization of NPR1, which is essential for SA-mediated defense gene expression, is not required for the suppression of JA signaling, indicating that cross-talk between SA and JA is modulated through a novel function of NPR1 in the cytosol.


Assuntos
Proteínas de Arabidopsis/fisiologia , Ciclopentanos/metabolismo , Defensinas , Proteínas Nucleares , Ácido Salicílico/metabolismo , Transdução de Sinais/fisiologia , Proteínas de Arabidopsis/genética , Sequência de Bases , Fatores de Transcrição de Zíper de Leucina Básica , Citosol/metabolismo , Proteínas de Ligação a DNA/genética , Proteínas de Ligação a DNA/metabolismo , Regulação da Expressão Gênica de Plantas/efeitos dos fármacos , Imunidade Inata/genética , Imunidade Inata/fisiologia , Lipoxigenase/genética , Lipoxigenase/metabolismo , Dados de Sequência Molecular , Oxilipinas , Doenças das Plantas/microbiologia , Proteínas de Plantas/genética , Proteínas de Plantas/metabolismo , Pseudomonas/crescimento & desenvolvimento , Ácido Salicílico/farmacologia , Transdução de Sinais/genética , Fatores de Transcrição/genética , Fatores de Transcrição/metabolismo
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