auxin transport
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Author(s):  
Alejandra Serrano ◽  
Nathalie Kuhn ◽  
Franko Restovic ◽  
Carlos Meyer-Regueiro ◽  
Mónica Madariaga ◽  
...  

2021 ◽  
Author(s):  
Lin Tao ◽  
Yingming Feng ◽  
Yalin Li ◽  
Xuewen Li ◽  
Xiaodong Meng ◽  
...  

AbstractThis study tested a hypothesis that boron (B) supply alleviates aluminum (Al) toxicity by modifying auxin distribution in functionally different root zones. Auxin distribution and transport at various Al and B ratios were analyzed using the range of molecular and imaging techniques. Al stress resulted in increased auxin accumulation in root apical meristem (MZ) and transition zones (TZ) while reducing its content in elongation zone (EZ). This phenomenon was explained by reduction in basipetal auxin transport caused by Al blockage of PIN2 endocytosis, regulated at posttranscriptional level. This inhibition of PIN2 endocytosis was dependent on actin filaments and microtubules. B supply facilitated the endocytosis and exocytosis of PIN2 carriers via recycling endosomes conjugated with IAA to modify Al-induced auxin depletion in the EZ. However, disruption of auxin signaling with auxinole did not alleviate Al-induced inhibition of root growth. B supply alleviates Al-induced inhibition of root growth via restoring the endocytic recycling of PIN2 proteins involved in the basipetal (shootward) auxin transport, restoring Al-induced auxin depletion in the elongation zone.Short summaryAluminum-intensified PIN2 abundance, nontranscriptional, via repressing PIN2 endocytosis to block polar auxin transport, and this adverse effect could be alleviated by boron supply.


2021 ◽  
Author(s):  
Nguyen Manh Linh ◽  
Enrico Scarpella

To form tissue networks, animal cells migrate and interact through proteins protruding from their plasma membranes. Plant cells can do neither, yet plants form vein networks. How plants do so is unclear, but veins are thought to form by the coordinated action of the polar transport and signal transduction of the plant hormone auxin. However, plants inhibited in both pathways still form veins. Patterning of vascular cells into veins is instead prevented in mutants lacking the function of the GNOM (GN) regulator of auxin transport and signaling, suggesting the existence of at least one more GN-dependent vein-patterning pathway. Here we show that pathway depends on the movement of an auxin signal through plasmodesmata (PDs) intercellular channels. PD permeability is high where veins are forming, lowers between veins and nonvascular tissues, but remains high between vein cells. Impaired ability to regulate PD aperture leads to defects in auxin transport and signaling, ultimately leading to vein patterning defects that are enhanced by inhibition of auxin transport or signaling. GN controls PD aperture regulation, and simultaneous inhibition of auxin signaling, auxin transport, and regulated PD aperture phenocopies null gn mutants. Therefore, veins are patterned by the coordinated action of three GN-dependent pathways: auxin signaling, polar auxin transport, and movement of an auxin signal through PDs. We have identified all the key vein-patterning pathways in plants and an unprecedented mechanism of tissue network formation in multicellular organisms.


2021 ◽  
pp. 153594
Author(s):  
Ana Cecilia Aliaga Fandino ◽  
Christian S. Hardtke
Keyword(s):  

2021 ◽  
Author(s):  
Jie Liu ◽  
Roberta Ghelli ◽  
Maura Cardarelli ◽  
Markus Geisler

AbstractDespite clear evidence that a local accumulation of auxin is likewise critical for male fertility, much less is known about the components that regulate auxin-controlled stamen development.In this study, we analyzed physiological and morphological parameters in mutants of key players of ABCB-mediated auxin transport and spatially and temporally dissected their expression on the protein level as well as auxin fluxes in the Arabidopsis stamens. Our analyses revealed that the FKBP42, TWISTED DWARF1 (TWD1), promotes stamen elongation and, to a lesser extent, anther dehiscence, as well as pollen maturation and thus is required for seed development. Most of the described developmental defects in twd1 are shared with the abcb1 abcb19 mutant, which can be attributed to the fact that TWD1 - as a described ABCB chaperon - is a positive regulator of ABCB1 and ABCB19-mediated auxin transport. However, reduced stamen number was dependent on TWD1 but not on investigated ABCBs, suggesting additional actors down-stream of TWD1. We predict an overall housekeeping function for ABCB1 during earlier stages, while ABCB19 seems to be responsible for the key event of rapid elongation at later stages of stamen development. Our data indicate that TWD1 controls stamen development by differential activation of ABCB-mediated auxin transport in the stamen.HighlightBy using a mix of phenotypical and imaging analyses, we here identify and functionally characterize a new master regulator of flower development.


2021 ◽  
Author(s):  
Yucong Li ◽  
Jiahui Shao ◽  
Yansong Fu ◽  
Yu Chen ◽  
Hongzhe Wang ◽  
...  

2021 ◽  
Author(s):  
Giovanni Giuliano ◽  
Yacong Cao ◽  
Kang Zhang ◽  
Hailong Yu ◽  
Donghui Xu ◽  
...  

Abstract Pepper (Capsicum spp.) is one of the earliest domesticated crops, providing a unique pungent sensation when eaten. Through the construction of the first pepper variome, we describe the main groups that emerged during domestication and breeding of C. annuum, their relations and temporal succession, and the molecular events underlying the main transitions. The initial differentiation in fruit shape and pungency, increase in fruit weight, and transition from erect to pendent fruits, and the recent appearance of blocky, large, sweet fruits (bell peppers), were accompanied by strong selection/fixation of key alleles and introgressions in two large genomic regions. Furthermore, we describe the identification of Up, a key domestication gene controlling erect vs pendent fruit orientation, encoding a BIG GRAIN protein involved in auxin transport, and Flip1 associated with capsaicinoid content, encoding a protein involved in phospholipid flipping. The function of Up was confirmed by virus-induced gene silencing. These findings constitute a cornerstone for understanding the domestication and differentiation of a key horticultural crop.


Weed Science ◽  
2021 ◽  
pp. 1-26
Author(s):  
Andrew R. S. de Queiroz ◽  
Carla A. Delatorre ◽  
Catarine Markus ◽  
Felipe R. Lucio ◽  
Paula S. Angonese ◽  
...  

Abstract In 2015, plants of Sumatran fleabane [Conyza sumatrensis (Retz.) E. Walker] were identified in a crop field with an unusual rapid necrosis herbicide symptom after application of 2,4-D. An initial study identified that the symptoms began about 2 h after herbicide application, the resistant factor is high (resistance factor = 19), and the resistance decreased at low light. The mechanism of resistance is not known yet, but the symptomatology suggests it may be related to reduced translocation, ATP-binding cassette class B (ABCB) transporters, changes on auxin perception genes or induction of genes involved in response to pathogens and abiotic stresses. The objective of this study was to investigate the mechanisms involved in the resistance to 2,4-D caused by rapid necrosis using inhibitors of enzymes involved in detoxification and carriers. Neither the inhibitors of ABCB and auxin transporters TIBA, NPA, verapamil and orthovanadate, nor the inhibitors of detoxifying enzymes, as malathion, NBD-Cl and imidazole, avoided the rapid necrosis phenotype. However, orthovanadate and sodium azide (possibly related with auxin transport) were able to partially reduce oxidative stress in leaf disc. The expression of ABCM10 (an ABCD transporter gene), TIR1_1 (an auxin receptor gene) and CAT4 (an amino acid transporter gene) was quickly reduced after 2,4-D application in the resistant accession. Contrary to our hypothesis, LESION SIMULATING DISEASE RESISTANCE 1_3 (LSD1_3) expression increased in response to 2,4-D. LSD1_3 is important for the response to pathogen and abiotic stresses. The rapid necrosis mechanism is not related to 2,4-D detoxification but might be related to changes in the TIR receptor or auxin transport. Mutations in other transporters or in proteins involved in abiotic and pathogen stresses cannot be ruled out.


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