Growth regulation tailors plant development to its environment. A showcase is response to gravity, where shoots bend up and roots down 1 . This paradox is based on opposite effects of the phytohormone auxin, which promotes cell expansion in shoots, while inhibiting it in roots via a yet unknown cellular mechanism 2 . Here, by combining micro uidics, live imaging, genetic engineering and phosphoproteomics in Arabidopsis thaliana, we advance our understanding how auxin inhibits root growth. We show that auxin activates two distinct, antagonistically acting signalling pathways that converge on the rapid regulation of the apoplastic pH, a causative growth determinant. Cell surface-based TRANSMEMBRANE KINASE1 (TMK1) interacts with and mediates phosphorylation and activation of plasma membrane H + -ATPases for apoplast acidi cation, while intracellular canonical auxin signalling promotes net cellular H + -in ux, causing apoplast alkalinisation. The simultaneous activation of these two counteracting mechanisms poises the root for a rapid, ne-tuned growth modulation while navigating complex soil environment. MainAuxin, a major growth regulator in plants, acts oppositely in shoots and roots. In shoots, canonical/intracellular auxin TRANSPORT INHIBITOR RESPONSE1 (TIR1)/AUXIN-SIGNALING F-BOX (AFB) receptors by downstream transcriptional regulation activate H + -pumps to acidify the apoplast a promote cell elongation 3,4 , in accordance with the Acid Growth Theory, which postulates that low apoplastic pH promotes growth 5 . In roots of many species including Arabidopsis, auxin inhibits growth. These contrasting responses are the basis for positive versus negative bending of roots and shoots in response to gravity and light 1 . The inhibitory auxin effect in roots also involves TIR1/AFB receptors but its rapid timing points towards an unknown non-transcriptional signalling branch 6 . Besides, a cell surface-based pathway involving TMK1 regulates development 7 , including differential growth in the apical hook 8 , while its role in auxin-regulated root growth remains unclear. Hence, the auxin signalling mechanism and the downstream processes for regulating root growth remain elusive.In this study, we revealed antagonistic action of intracellular TIR1/AFB and cell surface TMK1 auxin signalling converging on regulation of apoplastic pH, which we con rm as the key cellular mechanism allowing immediate and sensitive root growth regulation. Growth inhibition correlates with H + -in uxAuxin rapidly inhibits root growth through a non-transcriptional branch of TIR1/AFB signalling 6 . Although several cellular processes, including cortical microtubule (CMT) reorientation 9,10 , vacuolar fragmentation 11 and apoplastic pH changes [12][13][14] have been implicated, the causal mechanism remains unidenti ed.

Ab uilt-in electric field in electrocatalyst can significantly accumulate higher concentration of NO 3 À ions near electrocatalyst surface region, thus facilitating mass transfer for efficient nitrate removal at ultra-lowconcentration and electroreduction reaction (NO 3 RR). Am odel electrocatalyst is created by stacking CuCl (111) and rutile TiO 2 (110) layers together,i nw hich ab uilt-in electric field induced from the electron transfer from TiO 2 to CuCl (CuCl_BEF) is successfully formed .T his built-in electric field effectively triggers interfacial accumulation of NO 3 À ions around the electrocatalyst. The electric field also raises the energy of key reaction intermediate *NO to lower the energy barrier of the rate determining step.ANH 3 product selectivity of 98.6 %, alow NO 2 À production of < 0.6 %, and mass-specific ammonia production rate of 64.4 h À1 is achieved, whicha re all the best among studies reported at 100 mg L À1 of nitrate concentration to date.

Plant meristems carry pools of continuously active stem cells, whose activity is controlled by developmental and environmental signals. After stem cell division, daughter cells that exit the stem cell domain acquire transit amplifying cell identity before they are incorporated into organs and differentiate. In this study, we used an integrated approach to elucidate the role of HECATE (HEC) genes in regulating developmental trajectories of shoot stem cells in Arabidopsis thaliana. Our work reveals that HEC function stabilizes cell fate in distinct zones of the shoot meristem thereby controlling the spatio-temporal dynamics of stem cell differentiation. Importantly, this activity is concomitant with the local modulation of cellular responses to cytokinin and auxin, two key phytohormones regulating cell behaviour. Mechanistically, we show that HEC factors transcriptionally control and physically interact with MONOPTEROS (MP), a key regulator of auxin signalling, and modulate the autocatalytic stabilization of auxin signalling output.

Background and Aims Hepatocellular carcinoma (HCC) is the third leading cause of cancer‐related deaths worldwide, hence a major public health threat. Pleomorphic adenoma gene like‐2 (PLAGL2) has been reported to play a role in tumorigenesis. However, its precise function in HCC remains poorly understood. Approach and Results In this study, we demonstrated that PLAGL2 was up‐regulated in HCC compared with that of adjacent nontumorous tissues and also correlated with overall survival times. We further showed that PLAGL2 promoted HCC cell proliferation, migration, and invasion both in vitro and in vivo. PLAGL2 expression was positively correlated with epidermal growth factor receptor (EGFR) expression. Mechanistically, this study demonstrated that PLAGL2 functions as a transcriptional regulator of EGFR and promotes HCC cell proliferation, migration, and invasion through the EGFR‐AKT pathway. Moreover, hypoxia was found to significantly induce high expression of PLAGL2, which promoted hypoxia inducible factor 1/2 alpha subunit (HIF1/2A) expression through EGFR. Therefore, this study demonstrated that a PLAGL2‐EGFR‐HIF1/2A signaling loop promotes HCC progression. More importantly, PLAGL2 expression reduced hepatoma cells’ response to the anti‐EGFR drug erlotinib. PLAGL2 knockdown enhanced the response to erlotinib. Conclusions This study reveals the pivotal role of PLAGL2 in HCC cell proliferation, metastasis, and erlotinib insensitivity. This suggests that PLAGL2 can be a potential therapeutic target of HCC.

The phytohormone auxin and its directional transport through tissues are intensively studied. However, a mechanistic understanding of auxin-mediated feedback on endocytosis and polar distribution of PIN auxin transporters remains limited due to contradictory observations and interpretations. Here, we used state-of-the-art methods to reexamine the auxin effects on PIN endocytic trafficking. We used high auxin concentrations or longer treatments versus lower concentrations and shorter treatments of natural (IAA) and synthetic (NAA) auxins to distinguish between specific and nonspecific effects. Longer treatments of both auxins interfere with Brefeldin A-mediated intracellular PIN2 accumulation and also with general aggregation of endomembrane compartments. NAA treatment decreased the internalization of the endocytic tracer dye, FM4-64; however, NAA treatment also affected the number, distribution, and compartment identity of the early endosome/trans-Golgi network (EE/TGN), rendering the FM4-64 endocytic assays at high NAA concentrations unreliable. To circumvent these nonspecific effects of NAA and IAA affecting the endomembrane system, we opted for alternative approaches visualizing the endocytic events directly at the plasma membrane (PM). Using Total Internal Reflection Fluorescence (TIRF) microscopy, we saw no significant effects of IAA or NAA treatments on the incidence and dynamics of clathrin foci, implying that these treatments do not affect the overall endocytosis rate. However, both NAA and IAA at low concentrations rapidly and specifically promoted endocytosis of photo-converted PIN2 from the PM. These analyses identify a specific effect of NAA and IAA on PIN2 endocytosis, thus contributing to its polarity maintenance and furthermore illustrate that high auxin levels have nonspecific effects on trafficking and endomembrane compartments.