In addition to the full-length transcript , a splice variant () of the auxin response factor gene has been reported. Here, we identified an intron-retaining variant of , , whose translated product is imported into the nucleus and has tissue-specific localization in By inducibly expressing each variant in flowers, we show that fully complements the short-stamen phenotype of the mutant and restores the expression of , encoding a key regulator of stamen elongation. By contrast, the expression of and had minor or no effects on stamen elongation and expression. Coexpression of and in both the wild type and caused premature anther dehiscence: We show that is responsible for increased expression of the jasmonic acid biosynthetic gene and that is responsible for premature endothecium lignification due to precocious expression of transcription factor gene Finally, we show that ARF8.4 binds to specific auxin-related sequences in both the and promoters and activates their transcription more efficiently than ARF8.2. Our data suggest that ARF8.4 is a tissue-specific functional splice variant that controls filament elongation and endothecium lignification by directly regulating key genes involved in these processes.
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http://dx.doi.org/10.1105/tpc.17.00840 | DOI Listing |
Cancers (Basel)
December 2024
Department of Oncology-Pathology, Karolinska Institutet, 171 64 Solna, Sweden.
The epithelial-to-mesenchymal transition (EMT) is a common feature in early cancer invasion. Increased vimentin is a canonical marker of the EMT; however, the role of vimentin in EMT remains unknown. To clarify this, we induced EMT in lung cancer cells with TGF-β1, followed by treatment with the vimentin-targeting drug ALD-R491, live-cell imaging, and quantitative proteomics.
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December 2024
Department of Biochemistry and Molecular Biology, LSU Health Shreveport, Shreveport, LA 71103, USA.
For nearly a century, fundamental observations that prostate cancer (PCa) cells nearly always require AR stimulation for sustained proliferation have led to a unidirectional quest to abrogate such a pathway. Similarly focused have been efforts to understand AR-driven processes in the context of elevated expression of its target genes, and much less so on products that become overexpressed when AR signaling is suppressed. Treatment with ARSI results in an increased expression of the TLK1B splice variant via a 'translational' derepression driven by the compensatory mTOR activation and consequent activation of the TLK1 > NEK1 > ATR > Chk1 and NEK1 > YAP axes.
View Article and Find Full Text PDFInt J Mol Sci
December 2024
Institute of Neurology, Department of Medical and Surgical Sciences, University Magna Graecia, 88100 Catanzaro, Italy.
Pathogenic variants are associated with neonatal epilepsies, ranging from self-limited neonatal epilepsy to -developmental and epileptic encephalopathy (DEE). In this study, next-generation sequencing was performed, applying a panel of 142 epilepsy genes on three unrelated individuals and affected family members, showing a wide variability in the epileptic spectrum. The genetic analysis revealed two likely pathogenic missense variants (c.
View Article and Find Full Text PDFExp Hematol
January 2025
Department of Neuroscience, Karolinska Institutet, 171 77 Stockholm, Sweden. Electronic address:
T-cell acute lymphoblastic leukemia (T-ALL), which constitutes of 10-15% of all pediatric ALL cases, is known for its complex pathology due to pervasive genetic and chromosomal abnormalities. Although most children are successfully cured, chromosomal rearrangements involving the KMT2A gene is considered a poor prognostic factor. In a cohort of 171 pediatric T-ALL samples we have studied differences in gene and splice variant patterns in KMT2A rearranged (KMT2A-r) T-ALL compared to KMT2A negative (KMT2A-wt) T-ALL samples.
View Article and Find Full Text PDFCells
December 2024
Department of Biology and Biochemistry, University of Houston, Houston, TX 77204, USA.
Podocytes express large-conductance Ca-activated K channels (BK channels) and at least two different pore-forming KCa1.1 subunit C-terminal splice variants, known as VEDEC and EMVYR, along with auxiliary β and γ subunits. Podocyte KCa1.
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