How Do Cells Repair Damaged Plants

A recent written report in PNAS by Asahina et al. (1) addresses the fascinating question of tissue repair in plants. According to contempo suggestions, plants and animals might share cellular mechanisms that allow regeneration of tissues later on harm (2). Nevertheless, plants and animals differ greatly in their manner of evolution and their power to answer to damage-inducing ecology factors (3). Terrestrial plants cannot move their whole body in response to environmental cues, and, because of their cell walls, they as well lack cellular mobility within the plant. This ways that plants must regenerate damaged tissue through cellular regeneration at the point of impairment. Traditionally, this regeneration was considered to occur by dedifferentiation of existing mature cells followed by cell division to form callus and differentiation to form the cellular constituents of the new tissue, although details of this process take been questioned recently (4).

Plants experience many types of tissue impairment, including that caused by herbivory and other forms of concrete wounding (e.grand., breakage because of wind or ice or trampling by animals). They take adult elaborate responses to this harm. For case, herbivory results in a suite of responses; some are fast-acting and local, whereas others may be quite long-lived and systemic in nature, assuasive the plant to develop a response at the whole-plant level to set on by item fauna species (v).

One of the simplest forms of impairment to plants is the splitting or laceration of tissue. This type of wounding is frequent nether both natural and agronomic conditions. Information technology is also common with some of our well-established horticultural and research techniques (eastward.thou., grafting). Indeed, grafting and the subsequent tissue repair have been vital for the identification of two new plant hormones over the last 5 years: the strigolactones for branching (6) and the floral stimulus or florigen for flowering (seven). Notwithstanding, the molecular basis of tissue repair has remained largely unknown. The newspaper by Asahina et al. (1) provides some welcome insights into the repair procedure, since it shows that two institute-specific transcription factors (TFs), ANAC071 and RAP2.6L, are strongly up-regulated on the upper (ANAC071) and lower (RAP2.6L) sides of an incision in the infloresence stem. When the expression of these TFs is down-regulated using chimeric repressor silencing technology (8), repair of the wound is inhibited, indicating the importance of the TFs for the repair process.

Chiefly, the piece of work by Asahina et al. (1) provides prove that the TFs are regulated by plant hormones, with a focus on auxin. This hormone also regulates TFs involved in root tissue repair after harm by light amplification by stimulated emission of radiation ablation (ix). In the present example (1), the possible involvement of auxin implies communication between other parts of the plant and the repair site. Auxin is a mobile hormone, moving down the stem in a polar transport stream, and molecular evidence is presented that auxin accumulates on the upper (acropetal) side of the incision and depletes on the lower (basipetal) side. This information is used to develop a model in which auxin regulates TFs, which and so initiate cell division in the pith and ultimately repair the wound (Fig. 1).

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Model of tissue repair in the Arabidopsis inflorescence stem based on the work by Asahina et al. (one). The differential command of the TFs ANACO71 and RAP2.6L in the upper and lower sides, respectively, of an incision and their suggested regulation past the found hormones auxin, ethylene, and jasmonic acid (JA) are shown along with associated synthesis genes.

Roles for other institute hormones are also suggested (1). The ethylene-insensitive ein2 mutant does not undergo the same repair every bit WT plants considering of a lack of cell division in the pith. The expression of ANAC071 is reduced in ein2 plants suggesting that wound-induced ethylene may raise the auxin response. Ethylene levels are non directly measured but are inferred from the expression of the ACS2 gene, one of a family of aminocyclopropane carboxylic acid synthase genes that regulates the rate-limiting step in ethylene biosynthesis.

Jasmonic acrid (JA), another constitute hormone, may also play a role (1). JA is a known regulator of plant responses to both biotic and abiotic stresses (10), and genes involved in its biosynthesis are up-regulated later on incision, which is shown by microarray and quantitative RT-PCR analyses (1). One such gene, the lipoxygenase factor LOX2, is upwardly-regulated below the incision in a like pattern to RAP2.6L, and awarding of methyl jasmonate up-regulates RAP2.6L expression. Although studies using the expression of biosynthesis genes to infer hormone levels demand to exist treated with extreme caution (11), it seems that wounding up-regulates this cistron independently of auxin (1).

Overall, these results provide a testable model of some of the early on molecular steps involved in tissue repair. Understanding the molecular targets of the TFs and moving beyond correlations to show the straight regulation of the TFs by the hormones implicated will get a long mode to elucidating the command of this essential institute response. Thus far, the furnishings of straight applying hormones on the expression of the TF genes are less impressive than the effects of stem incision (cutting) or decapitation (removal of material at the top of the stem, including flowers) (1). For example, in cutting stems, decapitation dramatically reduces ANAC071 expression, but applying auxin to the decapitation site does not significantly opposite that effect (figure 3 in ref. 1). Possibly, the dose used (1 mM auxin in lanolin paste) is inadequate to restore the auxin content of stems. In previous inquiry, a similar dose did non fully restore the auxin level to the level of intact stems, although the hormone was applied repeatedly (12). Similarly, applying ii mM methyl jasmonate has only a moderate event on RAP2.6L expression compared with cut (figure 5 in ref. 1).

The possible roles of other hormones in tissue repair also require examination. In an before paper, Asahina et al. (xiii) noted the importance of another growth-promoting hormone, gibberellin (GA), in the repair process. In that case, hypocotyls of tomato plant and cucumber were studied. In considering the issue of auxin vs. GA, it should be borne in mind that loftier auxin content can lead to high GA content, because auxin promotes GA synthesis and inhibits its deactivation (14, fifteen). However, in the tomato hypocotyl, the pattern of factor expression after cotyledon removal is non consistent with an auxin-mediated effect on GA levels (sixteen), indicating the importance of GA per se. It is suggested that, in hypocotyls, GA is a key factor in the reunion of cortical cells whereas, in the pith cells of inflorescence stems, auxin is a major player (i). In this context, it is worth noting that GA-deficient pea mutants can be easily grafted epicotyl to epicotyl and epicotyl to stalk (17), indicating that GA is not essential for tissue reunion in that system.

Information technology is as well possible that different TFs regulate the repair response in hypocotyls and inflorescence stems because, earlier this year, Iwase et al. (18) reported that another recently discovered TF gene, WIND1, is up-regulated in wounded Arabidopsis hypocotyls. This gene was suggested to act every bit a master regulator of dedifferentiation during wound repair (18). Similar RAP2.6L, WIND1 belongs

Overall, these results provide a testable model of some of the early on molecular steps involved in tissue repair.

to the apetela2/ethylene response factor TF family. Interestingly, WIND1 is non included in a list of genes upward-regulated past the wounding of Arabidopsis stems (1). Consistent with evidence that auxin may non exist the key factor in hypocotyl repair, WIND1 (unlike RAP2.6L) is apparently not responsive to auxin (eighteen). The work past Iwase et al. (18) implicated another hormone, cytokinin, in TF-mediated repair, simply this time the hormone seemed to act downstream and not upstream of WIND1.

Dissimilar plant organs are affected in unlike means by both physical impairment and predation, and these differences may explicate the occurrence of unlike repair mechanisms. For example, leaves and flowers are determinate in growth and practice not directly prevent the growth of other organs, and, therefore, repair is not essential, although protection from additional impairment/invasion is advantageous to the establish. However, the stem is essential for subsequent organ development (e.thousand., leaves, roots, flowers, and seeds) considering of its disquisitional role in connectivity, support, and nutrient transport. Although new shoots may arise from axillary buds if the upper stem is damaged, the consequences for the constitute may be much greater than if an individual determinate organ is damaged.

The involvement of cell partition in the repair procedure has been known or assumed for a long time, and implicating plant hormones in the reformation of tissues, peculiarly vascular tissues, is likewise not new (19). The contribution by Asahina et al. (1) is the label of specific TFs, which, according to their model, form a molecular link between plant hormones and the cell partition response in the pith. Their piece of work (1) provides a foundation for determining whether tissue repair is controlled by similar TFs and constitute hormones in different tissues and different plant taxa.

Acknowledgments

We thank Laura Quittenden for preparing Fig. ane.

Footnotes

The authors declare no conflict of interest.

Run across companion article on page 16128 of issue 38 in volume 108.

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