Fine-Tuning of MiR528 Accumulation Modulates Flowering Time in Rice

In plants,microRNA (miRNA) functions in the post-transcriptional repression of target mRNAs have been well explored.However,the mechanisms regulating the accumulation of miRNAs remain poorly under.stood.Here,we report that distinct mechanisms regulate accumulation of a monocot-specific miRNA,rice (Oryza sativa) miR528.At the transcriptional level,miR528 accumulated to higher levels in older plants than in young seedlings and exhibited aging-modulated gradual accumulation and diurnal rhythms in leaves;at the post-transcriptional level,aging also modulated miR528 levels by enhancing pri-miR528 alter.native splicing.We found that miR528 promotes rice flowering under long-day conditions by targeting RED AND FAR-RED INSENSITIVE2 (OsRFI2).Moreover,natural variations in the MIR528 promoter region caused differences in miR528 expression among rice varieties,which are correlated with their different binding affinities with the transcription factor OsSPL9 that activates the expression of miR528.Taken together,our findings reveal rice plants have evolved sophisticated modes fine-tuning miR528 levels and provide insight into the mechanisms that regulate MIRNA expression in plants.

VprBP mitigates TGF-β and Activin signaling by promoting Smurf1-mediated type Ⅰ receptor degradation

The transforming growth factor-β(TGF-β)family controls embryogenesis,stem cell differentiation,and tissue homeostasis.However,how post-translation modifications contribute to fine-tuning of TGF-βfamily signaling responses is not well understood.Inhibitory(I)-Smads can antagonize TGF-β/Smad signaling by recruiting Smurf E3 ubiquitin ligases to target the active TGF-βreceptor for proteasomal degradation.A proteomic interaction screen identified Vpr binding protein(VprBP)as novel binding partner of Smad7.Mis-expression studies revealed that VprBP negatively controls Smad2 phosphorylation,Smad2–Smad4 interaction,as well as TGF-βtarget gene expression.VprBP was found to promote Smad7–Smurf1–TβRI complex formation and induce proteasomal degradation of TGF-βtype I receptor(TβRI).Moreover,VprBP appears to stabilize Smurf1 by suppressing Smurf1 poly-ubiquitination.In multiple adult and mouse embryonic stem cells,depletion of VprBP promotes TGF-βor Activin-induced responses.In the mouse embryo VprBP expression negatively correlates with mesoderm marker expression,and VprBP attenuated mesoderm induction during zebrafish embryogenesis.Our findings thereby uncover a novel regulatory mechanism by which Smurf1 controls the TGF-βand Activin cascade and identify VprBP as a critical determinant of embryonic mesoderm induction.

Precise editing of methylated cytosine in Arabidopsis thaliana using a human APOBEC3Bctd-Cas9 fusion

Dear Editor,Precise editing of specific genomic sites holds great promise in basic research and modern crop breeding,and some cytosine base editors(CBEs)have been developed for this purpose(Komor et al.,2016;Zong et al.,2018).

OVOL1 inhibits breast cancer cell invasion by enhancing the degradation of TGF-β type I receptor

Ovo-like transcriptional repressor 1(OVOL1)is a key mediator of epithelial lineage determination and mesenchymal–epithelial transition(MET).The cytokines transforming growth factor-β(TGF-β)and bone morphogenetic proteins(BMP)control the epithelial–mesenchymal plasticity(EMP)of cancer cells,but whether this occurs through interplay with OVOL1 is not known.Here,we show that OVOL1 is inversely correlated with the epithelial–mesenchymal transition(EMT)signature,and is an indicator of a favorable prognosis for breast cancer patients.OVOL1 suppresses EMT.