Changes in structure and dimension of plasmodesmata in the phloem loading pathway in Tecoma capensis (Bignoniaceae) - locating the polymer trap

2021 ◽  
Vol 140 ◽  
pp. 76-86
Author(s):  
CEJ Botha ◽  
Nelisha Murugan
Keyword(s):  
2021 ◽  
Author(s):  
Richard Breia ◽  
Artur Conde ◽  
Hélder Badim ◽  
Ana Margarida Fortes ◽  
Hernâni Gerós ◽  
...  

Abstract Sugars Will Eventually be Exported Transporters (SWEETs) have important roles in numerous physiological mechanisms where sugar efflux is critical, including phloem loading, nectar secretion, seed nutrient filling, among other less expected functions. They mediate low affinity and high capacity transport, and in angiosperms this family is composed by 20 paralogs on average. As SWEETs facilitate the efflux of sugars, they are highly susceptible to hijacking by pathogens, making them central players in plant–pathogen interaction. For instance, several species from the Xanthomonas genus are able to upregulate the transcription of SWEET transporters in rice (Oryza sativa), upon the secretion of transcription-activator-like effectors. Other pathogens, such as Botrytis cinerea or Erysiphe necator, are also capable of increasing SWEET expression. However, the opposite behavior has been observed in some cases, as overexpression of the tonoplast AtSWEET2 during Pythium irregulare infection restricted sugar availability to the pathogen, rendering plants more resistant. Therefore, a clear-cut role for SWEET transporters during plant–pathogen interactions has so far been difficult to define, as the metabolic signatures and their regulatory nodes, which decide the susceptibility or resistance responses, remain poorly understood. This fuels the still ongoing scientific question: what roles can SWEETs play during plant–pathogen interaction? Likewise, the roles of SWEET transporters in response to abiotic stresses are little understood. Here, in addition to their relevance in biotic stress, we also provide a small glimpse of SWEETs importance during plant abiotic stress, and briefly debate their importance in the particular case of grapevine (Vitis vinifera) due to its socioeconomic impact.


1982 ◽  
Vol 69 (3) ◽  
pp. 734-739 ◽  
Author(s):  
Julia W. Maynard ◽  
William J. Lucas

2021 ◽  
Vol 22 (3) ◽  
pp. 1159
Author(s):  
Leszek A. Kleczkowski ◽  
Abir U. Igamberdiev

Free magnesium (Mg2+) is a signal of the adenylate (ATP+ADP+AMP) status in the cells. It results from the equilibrium of adenylate kinase (AK), which uses Mg-chelated and Mg-free adenylates as substrates in both directions of its reaction. The AK-mediated primary control of intracellular [Mg2+] is finely interwoven with the operation of membrane-bound adenylate- and Mg2+-translocators, which in a given compartment control the supply of free adenylates and Mg2+ for the AK-mediated equilibration. As a result, [Mg2+] itself varies both between and within the compartments, depending on their energetic status and environmental clues. Other key nucleotide-utilizing/producing enzymes (e.g., nucleoside diphosphate kinase) may also be involved in fine-tuning of the intracellular [Mg2+]. Changes in [Mg2+] regulate activities of myriads of Mg-utilizing/requiring enzymes, affecting metabolism under both normal and stress conditions, and impacting photosynthetic performance, respiration, phloem loading and other processes. In compartments controlled by AK equilibrium (cytosol, chloroplasts, mitochondria, nucleus), the intracellular [Mg2+] can be calculated from total adenylate contents, based on the dependence of the apparent equilibrium constant of AK on [Mg2+]. Magnesium signaling, reflecting cellular adenylate status, is likely widespread in all eukaryotic and prokaryotic organisms, due simply to the omnipresent nature of AK and to its involvement in adenylate equilibration.


2016 ◽  
Vol 172 (3) ◽  
pp. 1876-1898 ◽  
Author(s):  
R. Frank Baker ◽  
Kristen A. Leach ◽  
Nathanial R. Boyer ◽  
Michael J. Swyers ◽  
Yoselin Benitez-Alfonso ◽  
...  

1998 ◽  
Vol 95 (20) ◽  
pp. 12055-12060 ◽  
Author(s):  
R. Turgeon ◽  
R. Medville
Keyword(s):  

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