Cell expansion is an essential process in plant morphogenesis and is regulated by the coordinated action of environmental stimuli and endogenous factors, such as the phytohormones auxin and brassinosteroid. Although the biosynthetic pathways that generate these hormones and their downstream signaling mechanisms have been extensively studied, the upstream transcriptional network that modulates their levels and connects their action to cell morphogenesis is less clear. Here, we show that the miR319-regulated TCP (TEOSINTE BRANCHED1, CYCLODEA, PROLIFERATING CELL FACTORS) transcription factors, notably TCP4, directly activate transcription and integrate the auxin response to a brassinosteroid-dependent molecular circuit that promotes cell elongation in hypocotyls. Furthermore, TCP4 modulates the common transcriptional network downstream to auxin-brassinosteroid signaling, which is also triggered by environmental cues, such as light, to promote cell expansion. Our study links function with the hormone response during cell morphogenesis and shows that developmental and environmental signals converge on a common transcriptional network to promote cell elongation.
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http://dx.doi.org/10.1105/tpc.16.00360 | DOI Listing |
Biochem Genet
January 2025
Department of Gynecology, Women's Hospital, Zhejiang University School of Medicine, Hangzhou, China.
This study aimed to identify shared gene expression related to circadian rhythm disruption in polycystic ovary syndrome (PCOS) and non-alcoholic fatty liver disease (NAFLD) to discover common diagnostic biomarkers. Visceral fat RNA samples were collected from 12 PCOS and 14 non-PCOS patients, a sample size representing the clinical situation and sufficient to capture PCOS gene expression profiles. Along with liver transcriptome profiles from NAFLD patients, these data were analyzed to identify crosstalk circadian rhythm-related genes (CRRGs) between the diseases.
View Article and Find Full Text PDFHum Genomics
January 2025
Department of Biostatistics, Epidemiology and Informatics, Perelman School of Medicine, University of Pennsylvania, Richards Building B304, 3700 Hamilton Walk, Philadelphia, PA, 19104, USA.
Background: Disease comorbidities and longer-term complications, arising from biologically related associations across phenotypes, can lead to increased risk of severe health outcomes. Given that many diseases exhibit sex-specific differences in their genetics, our objective was to determine whether genotype-by-sex (GxS) interactions similarly influence cross-phenotype associations. Through comparison of sex-stratified disease-disease networks (DDNs)-where nodes represent diseases and edges represent their relationships-we investigate sex differences in patterns of polygenicity and pleiotropy between diseases.
View Article and Find Full Text PDFGenome Biol
January 2025
Cecil H. and Ida Green Center for Reproductive Biology Sciences, University of Texas Southwestern Medical Center, Dallas, TX, 75390, USA.
Background: Genetic studies have associated thousands of enhancers with breast cancer (BC). However, the vast majority have not been functionally characterized. Thus, it remains unclear how BC-associated enhancers contribute to cancer.
View Article and Find Full Text PDFSci Rep
January 2025
Department of Endocrinology, Second Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan, 250001, Shandong, China.
Obesity (OB) and atherosclerosis (AS) represent two highly prevalent and detrimental chronic diseases that are intricately linked. However, the shared genetic signatures and molecular pathways underlying these two conditions remain elusive. This study aimed to identify the shared diagnostic genes and the associated molecular mechanism between OB and AS.
View Article and Find Full Text PDFCell Rep Methods
January 2025
Department of Pathology, University of California, San Francisco, San Francisco, CA, USA; The Eli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research, University of California, San Francisco, San Francisco, CA, USA. Electronic address:
On Earth, iron is abundant, bioavailable, and crucial for initiating the first catalytic reactions of life from prokaryotes to plants to mammals. Iron-complexed proteins are critical to biological pathways and essential cellular functions. While it is well known that the regulation of iron is necessary for mammalian development, little is known about the timeline of how specific transcripts network and interact in response to cellular iron regulation to shape cell fate, function, and plasticity in the developing embryo and beyond.
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