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Description
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The recent Tansley review on silicon by Bélanger and colleagues (Coskun et al., 2019) must have come as a surprise to many in the field. The surprise being the views expressed and conclusions drawn by the authors. Over the last 30 years we, as many, have followed and largely admired the research on silicon in plants by the groups of Bélanger and Ma. During this period, and the publication of many papers on silicon in plants by these groups, the majority opinion of this Tansley review that silicon is not ‘an active cellular agent’ in plant physiology had previously not been explicitly expressed. One could proffer the alternative view that before this Tansley review the raison d’être of much of their research was in looking to identify silicon's role as an ‘active cellular agent’. The authors’ Tansley review on silicon's role in plants now centres upon the ‘apoplastic obstruction hypothesis’ in which silicon is described as an ‘extracellular prophylactic agent against biotic and abiotic stresses’. In short, Bélanger and colleagues now claim that the benefits of silicon in plants accrue due to its adventitious deposition in gaps between cells. In the Summary they suggest that ‘a major reinterpretation of silicon's role is therefore needed’ and proceed to delineate such in their Tansley review. However, the reinterpretation offered by Bélanger and colleagues is not novel and important research and appropriate attributions to prior research are missing from this Tansley review. A model that is wholly dependent upon the formation of a silica obstruction throughout apoplastic pathways will rely heavily upon understanding of biological silicification (Currie & Perry, 2007), the mechanism underlying the obstruction in this hypothesis. However, in this review the mechanism of formation and deposition of biogenic silica in plants received only scant attention with much important past and recent research either inexplicably by-passed or not appropriately cited (Mann et al., 1983; Perry & Fraser, 1991; Law & Exley, 2011; Guerriero et al., 2016, 2018; Brugiére & Exley, 2017; Kulich et al., 2018). This research, if appropriately included and cited, would certainly challenge the authors’ perceived novelty of their proposed model. Simply put, the authors did not address the question that is pivotal to their own hypothesis. ‘Why do some plants deposit biogenic silica in myriad different tissues (Fig. 1), whereas others only deposit silica in a limited number of specialised structures while some plants deposit little if any silica anywhere at all?’ While there is not yet an unequivocal answer to this question it has been addressed in some depth in the scientific literature (Hodson et al., 2005; Exley, 2015; Guerriero et al., 2018) and these studies, critical to their hypothesis, should have been appraised and cited accordingly. Due consideration of published literature would have informed Bélanger and colleagues that the ‘reinterpretation of silicon's role in plants’ emphasized in their Summary has, in fact, been underway for many years. The authors would have to question the novelty of their unifying model of silicon in plants. One of us has been researching silicon in biology for at least as long as the authors of this review and during these years has regularly expressed the mantra that the only biologically available form of silicon is silicic acid (Exley, 1998). Such can be considered as a sacred and scientific truth emanating from an understanding of the chemistry of silicic acid in natural environments. Bélanger and colleagues now, for the first time in print to our knowledge, agree. It is unfortunate that they did not appropriately attribute their own new understanding of silicon chemistry in general (Exley & Sjöberg, 2014) and acknowledge accordingly and especially with respect to super-saturated concentrations of silicic acid being cytotoxic (Exley, 2015). While it is pleasing to read that Bélanger and colleagues support this approach (as others will now surely follow them), it would have been pertinent for them in this review to recognize from where they took their new directions. Not everything in the review is revisionary. Bélanger and colleagues continue to call the class of membrane channels known as aquaporins, silicon transporters. The seminal research of Bélanger and Ma in particular has advanced understanding of the role of aquaporins (and similar water channels) in the movement of silicic acid in plants. It is, therefore, incongruous of these authors to criticize other researchers for creating ‘confusion’ about silicon in plants while continuing to perpetuate confusion by referring to aquaporins as transporters. Bélanger and colleagues have, at the very least, read our treatise on this subject and they must appreciate the biochemical difference between a channel and a transporter (Exley, 2015). Bélanger and colleagues consistently acknowledge in their Tansley review that silicon moves throughout the plant as monomeric, uncharged silicic acid. In doing so and thereby accepting the prevailing science, they must also accept that the movement of silicic acid is passive and not active and that this passive movement utilizes water channels not transporters. As leaders in the field, it is incumbent on them to use the correct biochemical nomenclature thereby avoiding widespread confusion (Marron et al., 2016). The authors continue this line to suggest that plants that accumulate silica should be defined, not as at present as to the silicon content of their tissues (Hodson et al., 2005), but as to which aquaporins or water channels predominate in their tissues. Again, they misunderstand biological silicification and the main factors that influence this process. For example, an important omission in their thinking is the role played by guttation. While the movement of silicic acid throughout plant tissues is a pre-requisite for biological silicification, it is not by itself a definition of biological silicification. Plants additionally require the ‘biochemistry of silicification’ for the adventitious deposition of silica to take place. In plants where this critical biochemistry is missing or lacking, silicic acid is not deposited as silica and leaves the plant through guttation. To understand silicon in plants one needs to understand biological silicification (Exley, 2015). Bélanger, in particular, has significantly added to our understanding of silicon's role in protecting plants against biotic stress. The obstructive hypothesis put forward in this review directly addresses this and yet recent research that supersedes and augments this theory is not acknowledged (Guerriero et al., 2018). By way of contrast the authors of this review have little experience in silicon and abiotic stress which may explain myriad omissions (Bayliss et al., 1994; Hodson & Evans, 1995). Their understanding of the chemistry of silicic acid, as delineated in this Tansley review, should have informed them that the only known chemistry, inorganic or organic, of silicic acid that could explain its benefits in plants is in its unique bioinorganic chemistry with aluminium in forming hydroxyaluminosilicates (Beardmore et al., 2016). Silicic acid protects against the toxicity of aluminium in all biota (Birchall et al., 1989), including plants. The toxicity of aluminium in plants is manifold displaying myriad phenotypes and its amelioration (direct and indirect) by silicic acid is similarly diversely manifested. The fact that the authors of this review state that aluminium is a ‘heavy metal’ may, in our view, explain their lack of insight in this area. The authors’ assertion that the deposition of silicic acid as biogenic silica may also have a role to play in silicon's defence against abiotic factors is almost certainly true, if not yet proven unequivocally. We would contend that the ‘apoplastic obstruction model’ proposed by Bélanger and colleagues in their Tansley review, far from being ‘unifying’ does not represent a novel development. A reappraisal of the published science is required. (2019-03-15)
***This entry has been automatically imported via OpenAlex by LIST harvest scripts. Please refer to https://doi.org/10.1111/nph.15752 for the original and latest version of the publication*** (2026-07-01)
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