Search bioRxiv⌕ Search

bioRxiv · 10.1101/2021.04.27.441570

Activation of ACC synthase 2/6 increases stomatal density and cluster on the Arabidopsis leaf epidermis during drought

Abstract

It is known that the transcription factor SPEECHLESS (SPCH) drives entry of epidermal cells into stomatal lineage, and that the activation of subtilisin-like protease SDD1 reduces stomatal density and cluster on the epidermis. However, there is still a big gap in our understanding of the relationship between stomatal development and the establishment of stomatal density and pattern, especially during drought. Interestingly, 1-aminocyclopropane-1-carboxylic acid (ACC) not only promotes stomatal development, but also is involved in the establishment of stomatal density and pattern. ACC generation comes from the activity of ACC synthase (ACS), while ACS activity could be mediated by drought. This work showed that the Arabidopsis SPCH activated ACS2/6 expression and ACC-dependent stomatal generation with an increase of stomatal density and cluster under drought conditions; and the possible mechanisms were that ACC-induced Ca2+ shortage in stomatal lineage reduced the inhibition of the transcription factor GT-2 Like 1 (GTL1) on SDD1 expression. These suggest that ACS2/6-dependent ACC accumulation integrated stomatal development with the establishment of stomatal density and pattern by mediating Ca2+ levels in stomatal lineage cells on the leaf epidermis, and this integration is directly related to the growth or survival of plants under escalated drought stress. HighlightACC synthase ACS2/6 activation integrated stomatal individual development with space setting between stomata by mediating Ca2+ levels in stomatal lineage on the leaf epidermis in response to drought.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Jia, M.-z., Liu, L.-y., Geng, C., Song, C.-p., Jiang, J.. 2021-04-27. Activation of ACC synthase 2/6 increases stomatal density and cluster on the Arabidopsis leaf epidermis during drought. https://doi.org/10.1101/2021.04.27.441570

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

Functional characterization of Rho GTPase activating proteins SYDE1 and SYDE2

The human genome encodes more than 60 proteins containing Rho GTPase activating protein (RhoGAP) domains, many of which remain understudied with respect to their target specificity and biological roles. SYDE1 and SYDE2 are two such orphan RhoGAPs, for which there are few studies characterizing their biochemical and cellular functions and conflicting reports identifying their cognate GTPases. We previously identified SYDE1 and SYDE2 in a screen for substrates of the c-Jun N-terminal kinases. Here, we show that SYDE1 and SYDE2 are preferentially phosphorylated by JNK1 relative to other mitogen-activated protein kinases (MAPKs) at sites proximal to a kinase docking region. Purified SYDE1 and SYDE2 are shown to have significant catalytic GAP activity toward RhoA, Rac1, and Cdc42. However, neither up- nor down-regulation of SYDE1/2 expression leads to detectable changes in bulk GTP loading of any of these GTPases. Nevertheless, we demonstrate that SYDE1 and SYDE2, in a partially GAP-dependent manner, increase cell spreading and number of focal adhesions, and promote more directionally persistent migration in HEK293 cells. Together, these findings establish SYDE1 and SYDE2 as robust JNK substrates with catalytic activity toward a set of Rho GTPases and reveal basic functions of SYDE1 and SYDE2 in regulating cell morphology, adhesion, and migration.

cell biology↗

The filopodial scaffold polyphosphate dictates cell adhesion-versus-invasion decisions

Inorganic polyphosphate (polyP) is an ancient polymer conserved across all life, serving cell type and location specific functions in every major compartment. Yet its role at the plasma membrane, where it accumulates to peak levels in many primary cells, is largely unknown. Here we identify polyP as a stabilizing component of filopodia, actin based membrane protrusions that govern cell adhesion, contact inhibition, and chemotaxis. Elevating cellular polyP increases filopodial stability and enhances cell adhesion, whereas reducing polyP accelerates filopodial disassembly and promotes cell migration. Mechanistically, we find that polyP acts as a structural filopodial scaffold, recruiting and organizing IRSp53, a membrane curvature inducing protein. We show that metastatic fibroblasts and breast cancer organoids carry markedly reduced and intracellularly reorganized polyP levels relative to their non transformed counterparts. Restoring endogenous polyP via lipid nanoparticle delivery suppresses their invasive phenotypes and reverses prometastatic gene expression signatures, implicating polyP as a primordial tumor suppressor.

cell biology↗

Mitochondrial transfer mediates metabolic communication between beta cells and islet macrophages

Pancreatic islet macrophages support islet homeostasis and adapt their metabolic program in response to environmental cues, including beta cell released factors. Intercellular mitochondrial transfer is a biological process that modulates cellular responses. To test whether beta cells, which are strongly secretory, transfer mitochondria to islet macrophages, we generated mice with beta cell-specific expression of mitochondrial GFP (PhAMfloxIns1Cre). We demonstrate that beta cells transfer mitochondria to islet macrophages in vivo and in vitro. Diabetogenic stressors did not alter the frequency of mitochondrial transfer and macrophages containing beta cell-derived GFP exhibit increased protein synthesis rates. RNA-seq identified upregulation of activity-regulated cytoskeleton associated protein (Arc) in macrophages receiving beta cell-derived mitochondria, while disruption of actin cytoskeleton dynamics prevented mitochondrial transfer. Together, these findings identify mitochondrial transfer as a previously unrecognized mechanism of beta cell-macrophage communication that may contribute to islet homeostasis and immune regulation.

cell biology↗