Biology subjects

Huang, X.-Q.

Publications and source records attributed to Huang, X.-Q..

3 recordsLinked to original sources

bioRxiv2025

Mechanosensitive channel PIEZO1 enhances endometrial decidualization via BECN1-dependent autophagy

The mechanosensitive ion channel PIEZO1 plays critical roles in physiological and pathological processes in response to various types of mechanical forces, including shear stress, stretch, and extracellular matrix (ECM) stiffness. Decidualization is crucial for a successful pregnancy, characterized by the differentiation of fibroblastic endometrial stromal cells into round, secretory decidual cells, along with the rapid remodeling of the ECM. Herein, we report that PIEZO1 plays a crucial role in enhancing decidualization in response to extracellular matrix (ECM) stiffness and cell contraction. Uterine-specific knockout of Piezo1 using Pgr-Cre in mice results in subfertility due to decidualization impairment in mid-late pregnancy. Silencing of PIEZO1 in human endometrial stromal cells also results in impaired decidualization. Treatment with the PIEZO1 agonist Yoda1 enhances decidualization in both in vivo and in vitro models. Stromal cells growing on ECM with 25 kPa stiffness display a better decidualization response than cells seeded on softer 2 kPa surface or harder surface of the regulator petri dish, and this difference is abolished by null of Piezo1. Consistent with PIEZO1 as a Ca2+ modulator, blocking of intracellular Ca2+ or pCaMKII significantly inhibits Yoda1-enhanced decidualization. Further investigation reveals that BECN1-dependent autophagy acts as the downstream of PIEZO1. Silencing of Beclin1 abolishes Yoda1-induced decidualization, while Tat-BECN1 fully rescues impaired decidualization caused by the lack of PIEZO1. Finally, the lower expression of PIEZO1 is associated with impaired decidualization in the endometrium of endometriotic baboons. In conclusion, we have uncovered a novel mechanism of decidualization that is regulated by PIEZO1-mediated mechanotransduction, providing further insight into decidualization studies. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=187 HEIGHT=200 SRC="FIGDIR/small/668790v1_ufig1.gif" ALT="Figure 1"> View larger version (68K): org.highwire.dtl.DTLVardef@2d25faorg.highwire.dtl.DTLVardef@186e56org.highwire.dtl.DTLVardef@1f3f61borg.highwire.dtl.DTLVardef@1a26bb7_HPS_FORMAT_FIGEXP M_FIG C_FIG

physiology↗

bioRxiv2022

Emission of floral volatiles is facilitated by cell-wall non-specific lipid transfer proteins

For volatile organic compounds (VOCs) to be released from the plant cell into the atmosphere, they have to cross the plasma membrane, the cell wall, and the cuticle. However, how these hydrophobic compounds cross the hydrophilic cell wall is largely unknown. Using biochemical and reverse-genetic approaches combined with mathematical modeling, we show that cell-wall localized non-specific lipid transfer proteins (nsLTPs) facilitate VOC emission. Out of three highly expressed nsLTPs in petunia petals, which emit high levels of phenylpropanoid/benzenoid compounds, only PhnsLTP3 contributes to the VOC export across the cell wall to the cuticle. A decrease in PhnsLTP3 expression reduces volatile emission and leads to VOC redistribution with less VOCs reaching the cuticle without affecting their total pools. This intracellular build-up of VOCs lowers their biosynthesis by feedback downregulation of phenylalanine precursor supply to prevent self-intoxication. Overall, these results demonstrate that nsLTPs are intrinsic members of the VOC emission network, which facilitate VOC diffusion across the cell wall.

plant biology↗

bioRxiv2021

Dynamic histone acetylation in floral volatile synthesis and emission in petunia flowers

Biosynthesis of secondary metabolites relies on primary metabolic pathways to provide precursors, energy, and cofactors, thus requiring coordinated regulation of primary and secondary metabolic networks. However, to date it remains largely unknown how this coordination is achieved. Using Petunia hybrida flowers, which emit high levels of phenylpropanoid/benzenoid volatile organic compounds (VOCs), we uncovered genome-wide dynamic deposition of histone H3 lysine 9 acetylation (H3K9ac) during anthesis as an underlying mechanism to coordinate primary and secondary metabolic networks. The observed epigenome reprogramming is accompanied by transcriptional activation, at gene loci involved in primary metabolic pathways that provide precursor phenylalanine, as well as secondary metabolic pathways to produce volatile compounds. We also observed transcriptional repression among genes involved in alternative phenylpropanoid branches that compete for metabolic precursors. We show that GNAT family histone acetyltransferase(s) (HATs) are required for the expression of genes involved in VOC biosynthesis and emission, by using chemical inhibitors of HATs, and by knocking down a specific HAT, ELP3, through transient RNAi. Together, our study supports that chromatin level regulatory mechanisms may play an essential role in activating primary and secondary metabolic pathways to regulate VOC synthesis in petunia flowers. HIGHLIGHTOur study shows that posttranslational modification of histones is essential for regulating the biosynthesis and emission of floral scent compounds, thus providing insights into chromatin level regulation of secondary metabolism.

plant biology↗