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PpCAD2 was originally isolated from the ‘Wangkumbae’ pear (Pyrus pyrifolia Nakai), and it encodes for cinnamyl alcohol dehydrogenase (CAD), which is a key enzyme in the lignin biosynthesis pathway. In order to verify the function of PpCAD2, transgenic tomato (Solanum lycopersicum) ‘Micro-Tom’ plants were generated using over-expression constructs via the agrobacterium-mediated transformation method. The results showed that the PpCAD2 over-expression transgenic tomato plant had a strong growth vigor. Furthermore, these PpCAD2 over-expression transgenic tomato plants contained a higher lignin content and CAD enzymatic activity in the stem, leaf and fruit pericarp tissues, and formed a greater number of vessel elements in the stem and leaf vein, compared to wild type tomato plants. This study clearly indicated that overexpressing PpCAD2 increased the lignin deposition of transgenic tomato plants, and thus validated the function of PpCAD2 in lignin biosynthesis.

A disorder in pears that is known as ‘hard-end’ fruit affects the appearance, edible quality, and market value of pear fruit. RNA-Seq was carried out on the calyx end of ‘Whangkeumbae’ pear fruit with and without the hard-end symptom to explore the mechanism underlying the formation of hard-end. The results indicated that the genes in the phenylpropanoid pathway affecting lignification were up-regulated in hard-end fruit. An analysis of differentially expressed genes (DEGs) identified three NAC transcription factors, and RT-qPCR analysis of PpNAC138, PpNAC186, and PpNAC187 confirmed that PpNAC187 gene expression was correlated with the hard-end disorder in pear fruit. A transient increase in PpNAC187 was observed in the calyx end of ‘Whangkeumbae’ fruit when they began to exhibit hard-end symptom. Concomitantly, the higher level of PpCCR and PpCOMT transcripts was observed, which are the key genes in lignin biosynthesis. Notably, lignin content in the stem and leaf tissues of transgenic tobacco overexpressing PpNAC187 was significantly higher than in the control plants that were transformed with an empty vector. Furthermore, transgenic tobacco overexpressing PpNAC187 had a larger number of xylem vessel elements. The results of this study confirmed that PpNAC187 functions in inducing lignification in pear fruit during the development of the hard-end disorder.

Background The steroidal hormones brassinosteroids (BRs) play important roles in plant growth and development. The pathway and genes involved in BR biosynthesis have been identified primarily in model plants like Arabidopsis , but little is known about BR biosynthesis in woody fruits such as pear. Results In this study, we found that applying exogenous brassinolide (BL) could significantly increase the stem growth and rooting ability of Pyrus ussuriensis . PcDWF1 , which had a significantly lower level of expression in the dwarf-type pear than in the standard-type pear, was cloned for further analysis. A phylogenetic analysis showed that PcDWF1 was a pear brassinosteroid biosynthetic gene that was homologous to AtDWARF1 . The subcellular localization analysis indicated that PcDWF1 was located in the plasma membrane. Overexpression of PcDWF1 in tobacco ( Nicotiana tabacum ) or pear ( Pyrus ussuriensis ) plants promoted the growth of the stems, which was caused by a larger cell size and more developed xylem than those in the control plants, and the rooting ability was significantly enhanced. In addition to the change in vegetative growth, the tobacco plants overexpressing PcDWF1 also had a delayed flowering time and larger seed size than did the control tobacco plants. These phenotypes were considered to result from the higher BL contents in the transgenic lines than in the control tobacco and pear plants. Conclusions Taken together, these results reveal that the pear BR biosynthetic gene PcDWF1 affected the vegetative and reproductive growth of Pyrus ussuriensis and Nicotiana tabacum and could be characterized as an important BR biosynthetic gene in perennial woody fruit plants.

The hard-end is a disorder of pear fruit, however, the mechanisms underlying its development remain unknown. In this study, we found that the hard-end fruit contained a higher transcript abundance level of ethylene-response factor 1b-like ( PpERF1b-like ) and released more ethylene compared to normal pear. In the ethephon treated normal fruit, flesh tissues accumulated more lignin together with elevated expression of PpERF1b-like . Overexpressing PpERF1b-like transiently in fruit and stably in callus increased lignin accumulation and the expression of lignin biosynthesis genes; the opposite results were observed in fruit showing repressed expression of PpERF1b-like . These results confirmed the role of PpERF1b-like in promoting hard-end formation through promoting lignin synthesis. This study provided valuable information for further clarifying the regulation of hard-end formation in pear.

Superficial scald of pear fruit is a physiological disorder that easily occurs during cold storage and seriously affects pear eating quality and commodity value. It is important to study the mechanism of superficial scald disorder. Our previous study reported that the incidence of superficial scald of calcium chloride (CaCl2)-treated pear fruit during storage was significantly lower than that of untreated fruit. In this study, we found that the accumulation of lignin in CaCl2-treated fruit was significantly lower than that of untreated fruit. The expression of the Pb4CL2 gene in the lignin synthesis pathway was downregulated in the CaCl2-treated fruit. The lignification level of the fruit overexpressing Pb4CL2 was significantly higher than that of the empty vector fruit. Therefore, we speculate that downregulation of Pb4CL2 after CaCl2 treatment plays an important role in CaCl2 inhibiting superficial scald disorder by affecting lignin accumulation in pear fruit.

Glyoxalase I (Gly I) is the first enzyme in the glutathionine-dependent glyoxalase pathway for detoxification of methylglyoxal (MG) under stress conditions. Transgenic tomato ‘Money Maker’ plants overexpressing tomato SlGlyI gene (tomato unigene accession SGN-U582631/Solyc09g082120.3.1) were generated and homozygous lines were obtained after four generations of self-pollination. In this study, SlGlyI- overepxressing line (GlyI), wild type (WT, negative control) and plants transformed with empty vector (ECtr, positive control), were subjected to Al-treatment by growing in Magnavaca’s nutrient solution (pH 4.5) supplemented with 20 µM Al 3+ ion activity. After 30 days of treatments, the fresh and dry weight of shoots and roots of plants from Al-treated conditions decreased significantly compared to the non-treated conditions for all the three lines. When compared across the three lines, root fresh and dry weight of GlyI was significant higher than WT and ECtr, whereas there was no difference in shoot tissues. The basal 5 mm root-tips of GlyI plants expressed a significantly higher level of glyoxalase activity under both non-Al-treated and Al-treated conditions compared to the two control lines. Under Al-treated condition, there was a significant increase in MG content in ECtr and WT lines, but not in GlyI line. Quantitative proteomics analysis using tandem mass tags mass spectrometry identified 4080 quantifiable proteins and 201 Al-induced differentially expressed proteins (DEPs) in root-tip tissues from GlyI, and 4273 proteins and 230 DEPs from ECtr. The Al-down-regulated DEPs were classified into molecular pathways of gene transcription, RNA splicing and protein biosynthesis in both GlyI and ECtr lines. The Al-induced DEPs in GlyI associated with tolerance to Al 3+ and MG toxicity are involved in callose degradation, cell wall components (xylan acetylation and pectin degradation), oxidative stress (antioxidants) and turnover of Al-damaged epidermal cells, repair of damaged DNA, epigenetics, gene transcription, and protein translation. A protein–protein association network was constructed to aid the selection of proteins in the same pathway but differentially regulated in GlyI or ECtr lines. Proteomics data are available via ProteomeXchange with identifiers PXD009456 under project title ‘25Dec2017_Suping_XSexp2_ITAG3.2’ for SlGlyI- overexpressing tomato plants and PXD009848 under project title ‘25Dec2017_Suping_XSexp3_ITAG3.2’ for positive control ECtr line transformed with empty vector.

To study the effect of adding NdCl 3 on the characteristics of micro-arc oxidation coating of TC4 titanium alloy, micro-arc oxidation was performed by adding different concentrations of NdCl 3 to the base electrolyte. The changes in the surface morphology, phase composition, abrasion resistance, corrosion resistance and erosion resistance of the MAO coating after the addition of NdCl 3 were investigated, utilizing SEM, XRD, XPS, multifunctional material surface tester, electrochemical workstation and autoclave testing methods. The results showed that adding an appropriate amount of NdCl 3 can increase the oxidation voltage and improved the surface morphology of the coating, and the main constituent phases of the coating were rutile TiO 2 , anatase TiO 2 and Nd 2 O 3 . When the concentration of 0.06 g L −1 was added, the thickness and hardness of the coating reached the maximum value of 25.1 μm and 540 HV, and the roughness and coefficient of friction reached the minimum value of 1.022 μm and 0.281. In addition, the corrosion current density and the corrosion rate reached the minimum value of 5.028 × 10 –9 A cm −2 and 1.673 × 10 –3  mm a −1 . Therefore, the coating had excellent abrasion and wear resistance. The erosion experiments indicated that the titanium alloy substrate and the corrosion rate of the MAO coating increased with the extension of the erosion time, and the addition of NdCl 3 could effectively improve the erosion resistance of the TC4 titanium alloy substrate.

To study the effect of adding NdCl.sub.3 on the characteristics of micro-arc oxidation coating of TC4 titanium alloy, micro-arc oxidation was performed by adding different concentrations of NdCl.sub.3 to the base electrolyte. The changes in the surface morphology, phase composition, abrasion resistance, corrosion resistance and erosion resistance of the MAO coating after the addition of NdCl.sub.3 were investigated, utilizing SEM, XRD, XPS, multifunctional material surface tester, electrochemical workstation and autoclave testing methods. The results showed that adding an appropriate amount of NdCl.sub.3 can increase the oxidation voltage and improved the surface morphology of the coating, and the main constituent phases of the coating were rutile TiO.sub.2, anatase TiO.sub.2 and Nd.sub.2O.sub.3. When the concentration of 0.06 g L.sup.-1 was added, the thickness and hardness of the coating reached the maximum value of 25.1 m and 540 HV, and the roughness and coefficient of friction reached the minimum value of 1.022 m and 0.281. In addition, the corrosion current density and the corrosion rate reached the minimum value of 5.028 x 10.sup.-9 A cm.sup.-2 and 1.673 x 10.sup.-3 mm a.sup.-1. Therefore, the coating had excellent abrasion and wear resistance. The erosion experiments indicated that the titanium alloy substrate and the corrosion rate of the MAO coating increased with the extension of the erosion time, and the addition of NdCl.sub.3 could effectively improve the erosion resistance of the TC4 titanium alloy substrate.

Summary Hard‐end, superficial scald and cork spot are prevalent physiological disorders in pear fruit, characterized by an increase in lignin deposition, which impairs the fruit quality and reduces farmer income. Although calcium deficiency is known to exacerbate symptoms of these lignin‐related disorders, the underlying mechanisms remain poorly understood. In this study, we aimed to elucidate the regulatory network through which calcium modulates lignin deposition‐induced physiological disorders, using hard‐end disorder as a model. Our results showed that WRKY46, a transcription factor, is upregulated in hard‐end fruit but downregulated by calcium treatment. WRKY46 directly activates the transcription of NAC187, which in turn activates the expression of CCR, promoting lignin accumulation. Furthermore, CML38, a calcium sensor protein, enhances the transactivation capacity of WRKY46 via physical interaction. Calcium disrupts the CML38/WRKY46‐NAC187‐CCR cascade, ultimately suppressing lignin biosynthesis. Additionally, the upregulation of WRKY46, CML38 and NAC187 correlates with reduced Ca2+ levels in the fruit. Collectively, these data suggest that the development of lignin‐related physiological disorders in pear fruit is mediated by the CML38/WRKY46‐NAC187‐CCR regulatory module, which is enhanced by reduced Ca2+ levels. This module plays a dual role in both lignin accumulation and Ca2+ level reduction, shedding new light on the role of calcium in modulating fruit quality.

Hard end, a disorder that occurs in pears, consists of the apparent protrusion of the calyx due to the retarded development of the tissues surrounding it. The Whangkeumbae ( Pyrus pyrifolia ) variety has shown severe hard end in recent years. The lignin content and the sclereid amount and size increased during the development of the affected fruit. The expression patterns of the lignin-associated genes indicated that PpCAD1 and PpCAD2 remained at high levels during the fruit development period and were enhanced in the fruits exhibiting hard end. After harvest, PpCAD1 and PpCAD2 accumulated in the hard end fruit during cold storage and reached higher levels than those in the control fruit, which agreed with the lignin content changes and the activities of the phenylalanine ammonia lyase (PAL), 4-coumarate:coenzyme A ligase (4CL), cinnamyl alcohol dehydrogenase (CAD), guaiacol peroxidase (G-POD), and syringaldazine peroxidase (S-POD) enzymes. The expression patterns of PpCAD1 and PpCAD2 were proportionate to the lignin content of hard end fruit during both development and the cold storage time; thus, it may play a role in the lignification of hard end fruit. The expression levels of PpPAL1 , PpPAL2 , Pp4CL1 , Pp4CL2 , PpPOD1 , PpPOD2, and PpPOD3 showed no correlation with the lignin content during fruit development and cold storage. After calcium chloride (CaCl 2 ) treatment, the lignin content of hard end fruit during cold storage was significantly decreased and the activities of the associated enzymes PAL, 4CL, CAD, G-POD, and S-POD were inhibited. PpCAD1 and PpCAD2 showed lower transcriptional levels in CaCl 2 -treated fruit. CaCl 2 treatment could reduce the Ca deficiency of the fruit and the hard end disorder, and it may regulate lignin synthesis by controlling PpCAD1 and PpCAD2 expression.