Root Cell Death Research Articles

Indications of programmed cell death in wheat roots upon exposure to silver nanoparticles

Programmed cell death (PCD) can occur at every developmental stage as a plant’s response to various biotic and abiotic environmental factors. Silver nanoparticles (AgNPs) are widely used in consumer products and possess antimicrobial properties, making them important in assessing nanoparticle effects on plants. In the present study, we examined the impact of AgNPs (0, 0.5, 1, 5, 10, and 20 mg L-1) on wheat root PCD by evaluating parameters such as the mitotic index, chromosomal behaviors, nuclear deformation, cytochrome c release, caspase-1-like activity, and the expression of cysteine protease genes (TaVPE4, TaMCA1, and TaMCA4). Our findings revealed a dose-dependent decrease in the mitotic index ratio and increased chromosomal abnormalities induced by AgNPs. Additionally, we observed various hallmarks of PCD, including chromatin condensation, slight DNA smear, reduction in mitochondrial inner membrane potential, and cytochrome c release to the cytoplasm as well as increased caspase-1-like activity and TaVPE4 gene expression. Notably, the gene expressions of TaMCA1 and TaMCA4 were found to be antagonistically regulated by AgNPs, further indicating the induction of PCD by AgNP treatment. Overall, our study provides evidence of AgNP-induced PCD in wheat roots, elucidating the involvement of cysteine protease genes in this process.

Effect of Auxin on Cadmium Toxicity-Induced Growth Inhibition in Solanum lycopersicum.

Auxins play crucial regulatory roles in plants coping with cadmium (Cd) stress. However, the regulatory mechanism by which auxins alleviate Cd toxicity in tomato seedlings remains unclear. Here, we demonstrate that exposure to Cd stress leads to dynamic changes in the auxin response in tomato roots, characterized by an initial increase followed by a subsequent weakening. Under Cd stress, tomato seedlings show primary root- and hypocotyl-growth inhibition, accompanied by the accumulation of Cd and reactive oxygen species (ROS) in the roots. The exogenous application of 1-naphthylacetic acid (NAA) does not mitigate the inhibitory effect of Cd toxicity on primary root growth, but it does significantly enhance lateral root development under Cd stress. Auxin transport inhibitors, such as 1-N-naphthylphthalamic acid (NPA) and 2,3,5-triiodobenoic acid (TIBA), aggravate the growth inhibition of primary roots caused by Cd stress. Additionally, lateral root development was inhibited by NPA. However, applying auxin synthesis inhibitors L-kynurenine (kyn) and yucasin alleviated the tomato root growth inhibition caused by Cd stress; between them, the effect of yucasin was more pronounced. Yucasin mitigates Cd toxicity in tomato seedlings by reducing Cd2+ absorption and auxin accumulation, strengthening ROS scavenging, and reducing cell death in roots. These observations suggest that yucasin potentially mitigates Cd toxicity and improves the tolerance of tomato seedlings to Cd stress.

Supplemental Silicon and Boron Alleviates Aluminum-Induced Oxidative Damage in Soybean Roots.

Aluminum (Al) toxicity in acidic soils is a major abiotic stress that negatively impacts plant growth and development. The toxic effects of Al manifest primarily in the root system, leading to inhibited root elongation and functionality, which impairs the above-ground organs of the plant. Recent research has greatly improved our understanding of the applications of small molecule compounds in alleviating Al toxicity. This study aimed to investigate the role of boron (B), silicon (Si), and their combination in alleviating Al toxicity in soybeans. The results revealed that the combined application significantly improved the biomass and length of soybean roots exposed to Al toxicity compared to B and Si treatments alone. Our results also indicated that Al toxicity causes programmed cell death (PCD) in soybean roots, while B, Si, and their combination all alleviated the PCD induced by Al toxicity. The oxidative damage induced by Al toxicity was noticeably alleviated, as evidenced by lower MAD and H2O2 accumulation in the soybean roots treated with the B and Si combination. Moreover, B, Si, and combined B and Si significantly enhanced plant antioxidant systems by up-regulating antioxidant enzymes including CAT, POD, APX, and SOD. Overall, supplementation with B, Si, and their combination was found to alleviate oxidative damage and reduce PCD caused by Al toxicity, which may be one of the mechanisms by which they alleviate root growth inhibition due to Al toxicity. Our results suggest that supplementation with B, Si, and their combination may be an effective strategy to improve soybean growth and productivity against Al toxicity.

Effects of acetic acid treatment on growth and pigment contents in barley

Acetic acid (AA) is an organic acid and has been widely used as food preservative and a dietary spice in vinegar form. In addition to its therapeutic uses in its vinegar form, AA attenuates inhibitory effects of stress in plants. However, in some plant species toxic effects of AA have been found. Therefore, in this study, 0, 2.5 and 5 mM concentrations of AA were applied to 2-day-old barley (Hordeum vulgare L. cv. Bornova-92) seedlings for 2 days in order to investigate the possible toxic effects of AA. After treatments, seedlings were grown in AA-free conditions for 2 days to recover. AA inhibited root and shoot growth; decreased water content, fresh weight, chlorophyll, pheophytin, and carotenoid contents. However, anthocyanin and flavonoid contents, as well as the levels of UV-absorbing compounds and UV-B marker increased in the leaves of AA-treated plants. AA increased hydrogen peroxide (H2O2) content in shoots and induced cell death in roots. Soluble carbohydrate content decreased in roots of AA-treated plants while insoluble carbohydrate content increased. Our results demonstrate that AA in young barley seedlings can exhibit its toxic effects through oxidative stress, which induced antioxidative response in the form of molecules with antioxidative activities. These effects persisted for 2 days after the removal of AA.

Extracellular nitric oxide sustains root surface redox activity and growth under sudden flooding-induced hypoxic conditions in barley root tips

Main conclusionNitric oxide sustains root tip surface redox activity and restricts lipid peroxidation-triggered cell death in the root tips.In order to gain more insight into the involvement of nitric oxide (NO) in plant response to sudden flooding-induced hypoxic stress, we studied the effect of two NO donors, sodium nitroprusside and S-nitroso-L-glutathione, on short-term partial submergence-induced root growth inhibition, alteration in root surface redox activity, lipid peroxidation and cell death in two barley cultivars (cv.) at their early seedling stage. The short-term hypoxic stress induces root growth arrest in cv. Karmel, accompanied by increased lipid peroxidation and cell death. By contrast, in cv. Slaven, short-term hypoxic conditions cause only reduced root growth rate, associated with elevated extracellular NO level in the root tips. The root tip surface redox activity decreases with the increasing timespan of hypoxic conditions in both cultivars; however, this decrease in redox activity started earlier and was greater in the cv. Karmel in comparison with cv. Slaven. Application of NO donors during hypoxic stress sustains the root redox activity and eliminates the hypoxia-induced lipid peroxidation, accompanied by a partial restoration of root growth after short-term hypoxic stress. These results suggest that extracellular NO plays a key role in maintaining the root tip surface redox activity and in the restriction of lipid peroxidation and cell death under short-term hypoxic stress in the root tips of barley seedlings.

Potential role of apple wood biochar in mitigating mercury toxicity in corn (Zea mays L.)

Mercury (Hg) is a very toxic decomposition-resistant metal that can cause plant toxicity through bioaccumulation and oxidative damage. Biochar, derived from organic waste and agricultural garbage, is an on-site modification technique that can improve soil health in heavy metals-polluted regions. The present experiment was designed to explore the role of apple biochar in the management of mercury toxicity in corn (Zea mays cv. ‘PL535’). Different levels of biochar derived from apple wood (0%, 2.5%, 5.0%, and 7.5% w/w) along with different Hg concentrations (0, 20, 40, and 60 mg/L) were used in the experiment that was based on a completely randomized design. Based on the results, HgCl2 at all rates reduced root and shoot dry weight and length, tolerance index, chlorophyll a and b content, the Hill reaction, and dissolved proteins and increased shoot and root Hg content (up to 72.57 and 717.56 times, respectively), cell death (up to 58.36%), MDA level (up to 47.82%), H2O2 (up to 66.33%), dissolved sugars, and proline. The results regarding enzymatic and non-enzymatic antioxidants revealed increases in total phenol and flavonoids content (up to 71.27% and 86.71%, respectively), DPPH free radical scavenging percentage, and catalase (CAT) and ascorbate peroxidase (APX) activity (up to 185.93% and 176.87%, respectively), in corn leaves with the increase in the Hg rate applied to the culture medium. The application of biochar to the substrate of the Hg-treated corns reduced Hg bioavailability, thereby reducing Hg accumulation in the roots (up to 76.88%) and shoots (up to 71.79%). It also reduced the adverse effect of Hg on the plants by increasing their shoot and root dry weight, photosynthesizing pigments, Hill reaction, and APX activity and reducing cell death, H2O2 content, and MDA content. The results reflected the capability of apple wood biochar at all rates in reducing Hg bioavailability and increasing Hg fixation in Hg-polluted soils. However, it was most effective at the rate of 7.5%.

Comparative study of stress generated by osmolytes on the growth, photosynthesis and metabolic responses in Nigellasativa

Several abiotic stresses generate osmotic stress which alters physio-biochemical and metabolic responses in plant. In the present experiment, the impact of different osmolytes on the germination, morphological, and physio-biochemical responses of Nigella sativa L. (black cumin) was investigated. Nigella seeds were subjected to treatments with sodium chloride (NaCl), polyethylene glycol (PEG-6000), mannitol, or sorbitol, resulting in a reduction of the osmotic potential in soil. The osmolyte treatments reduced germination traits (germination percentage, germination index, and vigour index) and seedling growth in treated plants. The decline in seedling establishment and growth is attributed to higher accumulation of various reactive oxygen species like hydrogen peroxide (H2O2) and superoxides (O2−) and lipid peroxidation in treated plants. Furthermore, osmolyte stress induced stomatal closure caused decline in water-related parameters (transpiration, stomatal conductance, internal CO2 concentration) which consequently restrained plant growth and development. In addition, Osmolyte treatments reduced the chlorophyll levels, and photosynthetic activity, while increasing proline and carbohydrate content. Protein, nitrate reductase, and carbonic anhydrase activities were depleted, and root cell death was elevated. To counteract this oxidative damage and mitigate stress, the plant enhances its antioxidant enzymatic defense. Notably, in the present study, the activity of catalase (CAT), superoxide dismutase (SOD), and peroxidase (POX) is upregulated to efficiently scavenge ROS and alleviate the impact of the stress. The current study demonstrated that different osmolytes elicit diverse effects on the morpho-physiological, biochemical, and metabolic responses of Nigella. Among the tested osmolytes, NaCl had the most pronounced and deleterious impact on the plant, followed by mannitol and sorbitol. On the other hand, PEG had the least toxic outcomes on the physiological processes and overall health of plant.

Iron toxicity in plants: A Review

Iron (Fe) is an essential micronutrient for plant growth and development, but excessive iron uptake can cause iron toxicity, leading to damage to plant cell membranes, reduced growth, yield, and overall health. This review paper discusses the issue of iron toxicity in plants, a common problem that affects crops such as rice, soybean, wheat, vegetables and is a common issue in Southeast Asia, Brazil, Africa, Australia, and the United States. Iron toxicity is more likely to occur in soils with high pH, high organic matter, or elevated levels of available iron. It discusses the various mechanisms that cause iron toxicity in plants, such as competition with other essential elements, oxidative stress, and changes in gene expression and phytohormones. The excess iron ions can cause damage to the root cells and the plasma membrane, leading to oxidative stress and increased production of reactive oxygen species (ROS). ROS can cause damage to cellular components, such as lipids, proteins, and DNA, leading to the death of root cells. Plants have specific mechanisms to take up iron, including transport proteins that are responsible for moving Fe2+ across the plasma membrane of root cells. Furthermore, it discusses the impact of iron toxicity on plant growth and development, including stunted growth, reduced root development, decreased water and nutrient uptake, and reduced photosynthetic activity. Highlights the importance of proper management of iron levels in soils to prevent iron toxicity and promote healthy plant growth.

A stratagem for primary root elongation under moderate salt stress in the halophyte Schrenkiella parvula.

Schrenkiella parvula, an Arabidopsis-related halophyte, grows around Lake Tuz (Salt) in Turkey and can survive up to 600 mM NaCl. Here, we performed physiological studies on the roots of S. parvula and A. thaliana seedlings cultivated under a moderate salt condition (100 mM NaCl). Interestingly, S. parvula germinated and grew at 100 mM NaCl, but germination did not occur at salt concentrations above 200 mM. In addition, primary roots elongated much faster at 100 mM NaCl, while being thinner with fewer roots hair, than under NaCl-free conditions. Salt-induced root elongation was due to epidermal cell elongation, but meristem size and meristematic DNA replication were reduced. The expression of genes related to auxin response and biosynthesis was also reduced. Application of exogenous auxin abolished the changes in primary root elongation, suggesting that auxin reduction is the main trigger for root architectural changes in response to moderate salinity in S. parvula. In A. thaliana seeds, germination was maintained up to 200 mM NaCl, but post-germination root elongation was significantly inhibited. Furthermore, primary roots did not promote elongation even under fairly low salt conditions. Compared to A. thaliana, cell death and ROS content in primary roots of salt-stressed plants were significantly lower in S. parvula. These changes in the roots of S. parvula seedlings may be an adaptive strategy to reach lower salinity by advancing into deeper soils, while being impaired by moderate salt stress. This article is protected by copyright. All rights reserved.

ETI signaling nodes are involved in resistance of Hawaii 7996 to Ralstonia solanacearum-induced bacterial wilt disease in tomato

ABSTRACT Bacterial wilt caused by the soil-borne pathogen Ralstonia solanacearum is a destructive disease of tomato. Tomato cultivar Hawaii 7996 is well-known for its stable resistance against R. solanacearum. However, the resistance mechanism of Hawaii 7996 has not yet been revealed. Here, we showed that Hawaii 7996 activated root cell death response and exhibited stronger defense gene induction than the susceptible cultivar Moneymaker after R. solanacearum GMI1000 infection. By employing virus-induced gene silencing (VIGS) and CRISPR/Cas9 technologies, we found that SlNRG1-silenced and SlADR1-silenced/knockout mutant tomato partially or completely lost resistance to bacterial wilt, indicating that helper NLRs SlADR1 and SlNRG1, the key nodes of effector-triggered immunity (ETI) pathways, are required for Hawaii 7996 resistance. In addition, while SlNDR1 was dispensable for the resistance of Hawaii 7996 to R. solanacearum, SlEDS1, SlSAG101a/b, and SlPAD4 were essential for the immune signaling pathways in Hawaii 7996. Overall, our results suggested that robust resistance of Hawaii 7996 to R. solanacearum relied on the involvement of multiple conserved key nodes of the ETI signaling pathways. This study sheds light on the molecular mechanisms underlying tomato resistance to R. solanacearum and will accelerate the breeding of tomatoes resilient to diseases.

Lipid peroxide-derived short-chain aldehydes promote programmed cell death in wheat roots under aluminum stress.

Lipid peroxidation is a primary event in plant roots exposed to aluminum (Al) toxicity, which leads to the formation of reactive aldehydes. Current evidence demonstrates that the resultant aldehydes are integrated components of cellular damage in plants. Here, we investigated the roles of aldehydes in mediating Al-induced damage, particularly cell death, using two wheat genotypes with different Al resistances. Aluminum treatment significantly induced cell death, which was accompanied by decreased root activity and cell length. Al-induced cell death displayed granular nuclei and internucleosomal fragmentation of nuclear DNA, suggesting these cells underwent programmed cell death (PCD). During this process, caspase-3-like protease activity was extensively enhanced and showed a significant difference between these two wheat genotypes. Further experiments showed that Al-induced cell death was positively correlated with aldehydes levels. Al-induced representative diagnostic markers for PCD, such as TUNEL-positive nuclei and DNA fragmentation, were further enhanced by the aldehyde donor (E)-2-hexenal, but significantly suppressed by the aldehyde scavenger carnosine. As the crucial executioner of Al-induced PCD, the activity of caspase-3-like protease was further enhanced by (E)-2-hexenal but inhibited by carnosine in wheat roots. These results suggest that reactive aldehydes sourced from lipid peroxidation mediate Al-initiated PCD probably through activating caspase-3-like protease in wheat roots.

Hydrogen sulfide upregulates the alternative respiratory pathway in mangrove plant Avicennia marina to attenuate waterlogging-induced oxidative stress and mitochondrial damage in a calcium-dependent manner.

Hydrogen sulfide (H2 S) is considered to mediate plant growth and development. However, whether H2 S regulates the adaptation of mangrove plant to intertidal flooding habitats is not well understood. In this study, sodium hydrosulfide (NaHS) was used as an H2 S donor to investigate the effect of H2 S on the responses of mangrove plant Avicennia marina to waterlogging. The results showed that 24-h waterlogging increased reactive oxygen species (ROS) and cell death in roots. Excessive mitochondrial ROS accumulation is highly oxidative and leads to mitochondrial structural and functional damage. However, the application of NaHS counteracted the oxidative damage caused by waterlogging. The mitochondrial ROS production was reduced by H2 S through increasing the expressions of the alternative oxidase genes and increasing the proportion of alternative respiratory pathway in the total mitochondrial respiration. Secondly, H2 S enhanced the capacity of the antioxidant system. Meanwhile, H2 S induced Ca2+ influx and activated the expression of intracellular Ca2+ -sensing-related genes. In addition, the alleviating effect of H2 S on waterlogging can be reversed by Ca2+ chelator and Ca2+ channel blockers. In conclusion, this study provides the first evidence to explain the role of H2 S in waterlogging adaptation in mangrove plants from the mitochondrial aspect.

Uranium triggers ferroptosis-like cell death in Vicia faba roots by increasing iron accumulation and inhibiting glutathione peroxidase activity

Uranium (U) is a non-essential and toxic element that can cause cell death in plants, but the mechanism is unclear. In the present study, we found that U triggered iron (Fe)- and reactive oxygen species (ROS)-dependent ferroptosis-like cell death in Vicia faba roots. The results showed that U entered V. faba root cells and even accumulated in the nucleus and organelles. U accumulation resulted in obvious changes in mitochondrial morphology, including shrunken shape, rupture of outer membrane, increased density of inner membrane and fuzzy crista. Compared with the control, the accumulation of Fe and ROS in V. faba roots increased after U exposure, while the peroxidase (POD) and glutathion peroxidase (GPX) activities decreased significantly, which was only 57.7% and 14.3% of control, respectively. Transcriptomic data showed that the expression of genes related to ROS production was mainly up-regulated (e.g. NDH , CCR , RbohB ), while the expression of genes related to ROS scavenging was mainly down-regulated (e.g. GPX4 , POD1 , POD7 ). These results led to excessive accumulation of ROS in root cells and triggered ferroptosis-like cell death. The key mechanism of U triggering ferroptosis-like cell death was to increase Fe accumulation and decrease GPX activity, so the cell death was promoted by addition of Fe (FeSO 4 and FeCl 3 ), and was inhibited by the lipophilic antioxidants [ferrostatin (Fer-1) and Vitamin E (VE)] and the Fe chelators [ciclopirox olamine (CPX)]. In conclusion, we demonstrated for the first time that U triggered ferroptosis-like cell death in V. faba roots. Our results provide a new insight for revealing the toxicological mechanism of U and other heavy metals in plants. • Uranium triggered ferroptosis-like cell death in Vicia faba roots. • Uranium accumulated in the nucleus and organelles after entering root cells. • Uranium induced iron accumulation and lipid peroxidation in Vicia faba roots. • Uranium severely inhibited GPX4 expression and glutathione peroxidase activity.

NAC32 alleviates magnesium toxicity-induced cell death through positive regulation of XIPOTL1 expression.

Abscisic acid–inducible NAC32 alleviates magnesium toxicity-mediated cell death in roots through direct regulation of XIPOTL1 expression in Arabidopsis.

Phytotoxicity and the molecular response in yttrium oxide nanoparticle-treated Arabidopsis thaliana seedlings.

Due to the widespread application of rare earth oxide nanoparticles in various fields, their release into the environment is inevitable, and their potential toxicity and ecological impact have become a concern. Yttrium oxide nanoparticles are important rare earth oxide nanoparticles; however, their impact on plants and the molecular mechanism underlying their influence on plant growth and development are unclear. In this study, we found that yttrium oxide nanoparticles at concentrations exceeding 2mM significantly inhibited the growth of Arabidopsis seedlings. Using Arabidopsis marker lines for auxin signaling, we found that the application of yttrium oxide nanoparticles resulted in disordered auxin signaling in root cells. Auxin signaling in the cells of the quiescent center and columella stem cells decreased, while auxin signaling in the cells of the stele was enhanced. In addition, trypan blue staining showed that yttrium oxide nanoparticles induced root cell death. Transcriptome analysis showed that the nanoparticles specifically inhibited the expression of lignin synthesis-related genes, activated the MAPK signaling pathway, and enhanced the ethylene and abscisic acid signaling pathways in plants. This study demonstrates the phytotoxicity of yttrium oxide nanoparticles at the molecular level in Arabidopsis, and it provides a new perspective on how plants respond to rare earth oxide stress.

Mechanistic assessment of tolerance to iron deficiency mediated by Trichoderma harzianum in soybean roots.

Iron (Fe) deficiency in soil is a continuing problem for soybean (Glycine max L.) production, partly as a result of continuing climate change. This study elucidates how Trichoderma harzianum strain T22 (TH) mitigates growth retardation associated with Fe-deficiency in a highly sensitive soybean cultivar. Soil TH supplementation led to mycelial colonization and the presence of UAOX1 gene in roots that caused substantial improvement in chlorophyll score, photosynthetic efficiency and morphological parameters, indicating a positive influence on soybean health. Although rhizosphere acidification was found to be a common feature of Fe-deficient soybean, the upregulation of Fe-reductase activity (GmFRO2) and total phenol secretion were two of the mechanisms that substantially increased the Fe availability by TH. Heat-killed TH applied to soil caused no improvement in photosynthetic attributes and Fe-reductase activity, confirming the active role of TH in mitigating Fe-deficiency. Consistent increases in tissue Fe content and increased Fe-transporter (GmIRT1, GmNRAMP2a, GmNRAMP2b and GmNRAMP7) mRNA levels in roots following TH supplementation were observed only under Fe-deprivation. Root cell death, electrolyte leakage, superoxide (O2 •- ) and hydrogen peroxide (H2 O2 ) substantially declined due to TH in Fe-deprived plants. Further, the elevation of citrate and malate concentration along with the expression of citrate synthase (GmCs) and malate synthase (GmMs) caused by TH suggest improved chelation of Fe in Fe-deficient plants. Results also suggest that TH has a role in triggering antioxidant defence by increasing the activity of glutathione reductase (GR) along with elevated S-metabolites (glutathione and methionine) to stabilize redox status under Fe-deficiency. TH increases the availability and mobilization of Fe by inducing Fe-uptake pathways, which appears to help provide resistance to oxidative stress associated with Fe-shortage in soybean. These findings indicate that while Fe deficiency does not affect the rate or degree of TH hyphal association in soybean roots, the beneficial effects of TH alone may be Fe deficiency-dependent.

Dynamic analysis of physiological indices and transcriptome profiling revealing the mechanisms of the allelopathic effects of phenolic acids on Pinellia ternata.

Pinellia ternata (Thunb.) is a famous traditional Chinese medicine with high medicinal value, but its culture is strongly hindered by the continuous cropping obstacles (CCO) which are tightly associated with allelopathic effects. Deciphering the response mechanisms of P. ternata to allelochemicals is critical for overcoming the CCO. Here, we elucidate the response of P. ternata to phenolic acids treatment via physiological indices, cellular approaches, and transcriptome analysis. Phenolic acids showed a significant effect on the growth of P. ternata seedlings, similar to the phenotype of continuous cropping. Cellular analysis demonstrated that phenolic acids remarkably induced root cell death. Physiological analysis revealed that phenolic acids induced the overaccumulated of H2O2 and in root cells. However, two exogenous antioxidants (L-ascorbic acid and β-gentiobiose) aid in the scavenging of over-accumulated H2O2 and by promoting the antioxidant enzyme activity such as superoxide dismutase (SOD), ascorbate peroxidase (APX), and catalase (CAT). Transcriptome analysis demonstrated that differentially expressed genes (DEGs) related to the cell wall degeneration and reactive oxygen species (ROS) metabolism were upregulated by phenolic acid treatment. In addition, downregulated DEGs involved in sucrose and starch metabolism and phenylpropanoid biosynthesis pathways decreased the key metabolites contents. Taken together, phenolic acids caused root cell death by inducing the overaccumulation of H2O2 and , and L-ascorbic acid and β-gentiobiose effectively alleviated ROS stress. The present study elucidates the underlying mechanism of the allelopathic effect of phenolic acids, offers valuable information for further understanding the mechanism of CCO, and could contribute to improving guidance for further P. ternata production.

Interference of Dihydrocoumarin with Hormone Transduction and Phenylpropanoid Biosynthesis Inhibits Barnyardgrass (Echinochloa crus-galli) Root Growth.

Botanical compounds with herbicidal activity exhibit safety, low toxicity, and low chances of herbicide resistance development in plants. They have widespread applications in green agricultural production and the development of organic agriculture. In the present study, dihydrocoumarin showed potential as a botanical herbicide, and its phenotypic characteristics and mechanism of action were studied in barnyardgrass [Echinochloa crus-galli (L.) P.Beauv.] seedlings. The results indicated that dihydrocoumarin inhibited the growth of barnyardgrass without causing significant inhibition of rice seedling growth at concentrations ranging between 0.5 and 1.0 g/L. Additionally, dihydrocoumarin treatment could cause oxidative stress in barnyardgrass, disrupt the cell membrane, and reduce the root cell activity, resulting in root cell death. Transcriptomic analyses revealed that dihydrocoumarin could inhibit barnyardgrass normal growth by affecting the signal transduction of plant hormones. The results showed significant differential expression of plant hormone signal transduction genes in barnyardgrass. Additionally, dihydrocoumarin interfered with the expression of numerous phenylpropanoid biosynthesis genes in barnyardgrass that affect the production of various vital metabolites. We speculate that the barnyardgrass growth was suppressed by the interaction among hormones and phenylpropanoid biosynthesis genes, indicating that dihydrocoumarin can be applied as a bioherbicide to control barnyardgrass growth in rice transplanting fields.

Autophagy alleviates indium-induced programmed cell death in wheat roots

Indium released in agroecosystems is becoming an emerging plant stressor, causing cellular damage and consequently crop yield losses. Previous studies have focused on indium-induced toxicity in plants, while plant adaptive responses to such emerging metal xenobiotics are poorly understood. Here, we explored the relationship of autophagy and programmed cell death (PCD) in wheat roots under indium stress. Indium treatment significantly decreased root activity and cell viability, and suppressed the length of root epidermal cells in the elongation zones. These symptoms may be associated with indium-induced PCD, as indium-stressed wheat roots displayed condensed and granular nuclei, increased number of TUNEL-positive nuclei, enhanced nuclear DNA fragmentation and caspase-3-like protease activity compared to untreated roots. Accordingly, indium enhanced the expression levels of TaMCA1 and TaMCA4, two major metacaspase genes mediated PCD in wheat plants. The enhanced expression of autophagy genes and formation of autophagosomes indicate that autophagy could regulate metabolic adaptation and repair stress-induced damage in wheat roots. Furthermore, reinforcing autophagy by activator rapamycin significantly decreased the number of TUNEL-positive nuclei and the activity of caspase-3-like protease, whereas inhibition of autophagy by 3-methyladenine aggravated diagnostic markers for PCD. These results together suggest that autophagy suppresses indium-induced PCD in wheat roots.

Nitric oxide and hydrogen peroxide independently act in mitigating chromium stress in Triticum aestivum L. seedlings: Regulation of cell death, chromium uptake, antioxidant system, sulfur assimilation and proline metabolism

In this study, we have explored potential of a nitric oxide (NO) donor (SNP, sodium nitroprusside) and hydrogen peroxide (H2O2) in curtailing stress of hexavalent chromium [Cr(VI)] in wheat seedlings. Cr(VI) stress caused a significant decline in growth (30%) and photosynthesis (13%) as a result of enhanced uptake of Cr(VI) and root tips cell death. Further, Cr(VI) stress also accelerated indices of oxidative stress but differentially regulated antioxidant system. But application of either NO or H2O2 separately significantly mitigated Cr(VI) stress by reducing cell death and Cr(VI) uptake in roots, and oxidative stress markers. The application of c-PTIO [2-(4-carboxy-2-phenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide, a scavenger of NO] and N-acetyl-L-cysteine (a scavenger of ROS) reserved alleviatory effect of NO and H2O2, respectively and thus further increased Cr(VI) toxicity. Application of diphenylene iodonium (DPI, an inhibitor of NADPH oxidases) also further increased Cr(VI) toxicity. But SNP and H2O2 significantly rescued negative effects of DPI and c-PTIO, respectively under Cr(VI) stress. Overall results suggested that NO and H2O2 both independently act in mitigating Cr(VI) stress in wheat seedlings by minimizing cell death, restricting Cr(VI) uptake in roots, and increasing antioxidant system, sulfur assimilation and proline metabolism.