Skinning Injury Responses in Sweetpotato

In sweetpotatoes (Ipomoea batatas L. Lamb), the loss of skin from the surface of the storage roots is known as skinning injury. It is responsible for significant postharvest loss resulting from moisture increase and weight reduction, wrinkling, and susceptibility to pathogen attack. Reduced root weight by water loss is associated with a higher rate of rot predominantly occurred in the developing and underdeveloped countries which can count of 8-20% of postharvest loss. Plants have different adaptation to protect themselves against skinning injury. Lignification, suberization, and increased sugar at the wound site have been shown to be correlated with wound healing. Changing in gene expressions have been associated with skinning injury. Genes associated in the biosynthesis of lignin and suberin, protein fate, cell-wall modification, transcription and protein synthesis, and stress responses and defense have been associated with skinning injury responses in plants. Understanding the skinning injury responses and how to regulate them can be used to produce a more desirable plant resistant to skinning injury. This paper especially reviews and discusses skinning injury responses in sweetpotato, a root crop which product may severely be affected by skinning injury. Keywords: gene expression, Ipomoea batatas, lignification, postharvest loss, wounding   ABSTRAK Pada ubi jalar (Ipomoea batatas L. Lamb), cedera kulit adalah hilangnya kulit dari permukaan umbi. Cedera kulit ini bertanggung jawab atas kerugian pascapanen yang signifikan akibat peningkatan laju kelembaban dan penurunan berat umbi, pengerutan, dan kerentanan terhadap serangan patogen. Berat umbi yang berkurang karena kehilangan air dikaitkan dengan tingkat pembusukan yang lebih tinggi, terutama terjadi di negara-negara berkembang dan yang kurang berkembang dengan kehilangan hasil panen umbi 8-20%. Tanaman memiliki adaptasi yang berbeda untuk melindungi diri dari cedera kulit. Lignifikasi, suberisasi, dan peningkatan gula di lokasi pelukaan telah terbukti berkorelasi dengan penyembuhan luka. Perubahan ekspresi gen telah dikaitkan dengan cedera kulit. Gen-gen yang terlibat dalam jalur biosintesis lignin dan suberin, protein tujuan akhir, modifikasi dinding sel, transkripsi dan sintesis protein, serta respons stres dan pertahanan telah dikaitkan dengan respons cedera kulit pada tanaman. Memahami respons cedera kulit dan bagimana cara mengaturnya dapat digunakan untuk menghasilkan tanaman yang diinginkan yang tahan terhadap cedera kulit umbi. Paper ini secara khusus mengulas dan membahas respon cedera kulit pada ubi jalar, suatu tanaman umbian yang hasilnya sangat terpengaruh oleh cedera kulit. Kata kunci: ekspresi gen, Ipomoea batatas, lignifikasi, kehilangan pascapanen, pelukaa

Differential gene expression of resistant and susceptible sweetpotato plants after infection with the causal agents of sweet potato virus disease

Sweet potato virus disease (SPVD) is one of the most devastating diseases affecting sweetpotato (Ipomoea batatas), an important food crop in developing countries. SPVD develops when sweetpotato plants are dually infected with sweet potato feathery mottle virus (SPFMV) and sweet potato chlorotic stunt virus (SPCSV). To better understand the synergistic interaction between these viruses, global gene expression was previously studied in the susceptible cultivar Beauregard. In the current study, global gene expression between SPVD-affected plants and virus-tested control plants (VT) were compared in \u27Beauregard\u27 (Bx) and resistant \u27NASPOT 1\u27 (Nas) sweetpotato cultivars at 5, 9, 13, and 17 days post inoculation (DPI). Titer levels of SPFMV and SPCSV were significantly lower in inoculated resistant plants (Nas_SPVD) than in susceptible plants (Bx_SPVD) at most of the time points. Chloroplast genes and cell expansion-related genes (including xyloglucan endotransglucosylase/hydrolases) were suppressed in Bx_SPVD, while stress-related genes were induced. This trend was not observed in resistant NAS_SPVD. Genes related to protein synthesis (e.g., ribosomal proteins and elongation factor genes) were induced in resistant NAS_SPVD at 5 DPI before returning to levels comparable with NAS_VT plants. At this time (5 DPI), individual viruses could not be detected in NAS_SPVD samples, and no symptoms were observed. Induction of protein synthesis-related genes is common in susceptible plants after virus infection and is generally in proportion to virus accumulation. Our results show that induction of protein synthesis genes also occurs early in the infection process in resistant plants, while virus titers were below the level of detection, suggesting that virus accumulation is not required for induction

Field performance of tissue-cultured, virus-tested ‘okinawan’ sweetpotato and comparison with some promising cultivars in hawai’i

Tissue-cultured, virus-tested (TC) plantlets of sweetpotato (Ipomoea batatas var. batatas) cultivars Okinawan, LA 08-21p, and Murasaki-29 were obtained from Louisiana State University Agricultural Center. The objectives of field trials conducted at the Kula Agricultural Park, Maui, HI, were to compare yield and pest resistance of 1) ‘Okinawan’ obtained from a commercial (C) field with TC ‘Okinawan’ and 2) TC Okinawan with the aforementioned TC cultivars. Trials were planted Oct. 2015 and Aug. 2016 and harvested 5 months later. Storage roots were graded according to State of Hawai’i standards, and marketable yields included Grades AA, A, and B. In addition, injuries due to sweetpotato weevil (Cylas formicarius elegantulus) or rough sweetpotato weevil (Blosyrus asellus) were estimated. In both trials, fresh and dry weights of marketable storage roots of TC ‘Okinawan’ were nearly twice those from commercial planting material. In both trials, marketable fresh weights differed among the three TC cultivars; however, significant interactions were found, indicating that yields of cultivars differed between years. In the first field trial, ‘LA 08-21p’ had fresh marketable yields 1.6 to 1.7 times greater than TC ‘Okinawan’ and Murasaki-29, respectively. In the second trial, fresh marketable yields of TC ‘Okinawan’ and ‘LA 08-21p’were similar and 1.7 to 1.5 times greater than that of ‘Murasaki-29’, respectively. In both trials, ‘LA 08-21p’ had greater sweetpotato weevil injury than did the other two cultivars. Interestingly, in the second year, TC ‘Okinawan’ had greater rough sweetpotato weevil injury than did the other cultivars. Our results indicate that tissue-cultured planting materials increased marketable yields of TC ‘Okinawan’ compared with C ‘Okinawan’ sweetpotato and that the other TC cultivars did not produce greater yields than TC Okinawan

Differential expression of genes between storage roots of sweetpotato cultivars jewel and white jewel

\u27White Jewel\u27 is a yellow-and-orange fleshed spontaneous mutant of the orange-flesh sweetpotato [Ipomoea batatas (L.) Lam.] cultivar Jewel. Mutations in storage root flesh color, and other traits are common in sweetpotato. The orange flesh color of sweetpotato is due to β-carotene stored in chromoplasts of root cells. β-carotene is important because of its role in human health. In an effort to elucidate biosynthesis and storage of β-carotene in sweetpotato roots, microarray analysis was used to investigate genes differentially expressed between \u27White Jewel\u27 and \u27Jewel\u27 storage roots. β-carotene content calculated from a* color values of \u27Jewel\u27 and \u27White Jewel\u27 were 20.66 mg/100 g fresh weight (FW) and 1.68 mg/100 g FW, respectively. Isopentenyl diphosphate isomerase (IPI) was down-regulated in \u27White Jewel\u27, but farnesyl-diphosphate synthase (FPPS), geranylgeranyl diphosphate synthase (GGPS), and lycopene β-cyclase (LCY-b) were not differentially expressed. Several genes associated with chloroplasts were differentially expressed, indicating probable differences in chromoplast development of \u27White Jewel\u27 and \u27Jewel\u27. Sucrose Synthase was down-regulated in \u27White Jewel\u27 and fructose and glucose levels in \u27White Jewel\u27 were lower than in \u27Jewel\u27 while sucrose levels were higher in \u27White Jewel\u27. No differences were observed between dry weight or alcohol insoluble solids of the two cultivars. This study represents the first effort to elucidate β-carotene synthesis and storage in sweetpotato through large-scale gene expression analysis

Identification of molecular markers associated with sweet potato resistance to sweet potato virus disease in Kenya

Sweet potato virus disease (SPVD), a result of the co-infection of whitefly transmitted Sweet potato chlorotic stunt virus (genus Crinivirus, family Closteroviridae) and the aphid transmitted Sweet potato feathery mottle virus (genus Potyvirus, family Potyviridae), is the most destructive disease of sweet potato in East Africa. A study was conducted to establish if genotypes identified as resistant or susceptible to SPVD in Kenya could be distinguished using molecular markers. A total of 47 unrelated sweet potato genotypes were selected from germplasm collections and classified into two phenotypic groups as resistant or susceptible to SPVD. Genotype selection was based on disease severity or days to symptom development in plants following graft inoculation. Amplified fragment length polymorphism (AFLP) marker profiles were generated for each individual and used in association studies to identify markers suitable for classifying the two pre-defined phenotypic groups. Analysis of molecular variance showed significant (P \u3c 0.002) variation between the two groups using 206 polymorphic AFLP markers. Discriminant analysis and logistic regression statistical methods were used to select informative markers, and to develop models that would classify the two phenotypic groups. A training set of 30 genotypes consisting of 15 resistant and 15 susceptible were used to develop classification models. The remaining 17 genotypes were used as a test set. Four markers, which gave 100% correct classification of the training set and 94% correct classification of the test set, were selected by both statistical methods. © 2007 Springer Science+Business Media B.V

Molecular marker variability for southern root-knot nematode resistance in sweetpotato

Amplified fragment length polymorphism (AFLP) marker profiles for individuals in two F1 populations of sweetpotato [Ipomoea batatas (L.) Lam] were used in association studies to identify AFLP markers suitable for identification of plants possessing a resistant reaction to southern root-knot nematode race 3 [Meloidogyne incognita (Kofoid and White) Chitwood]. Population one consisted of 48 half-sib genotypes developed at the Louisiana State University (LSU) AgCenter. The second population consisted of 54 full-sibs developed by the East African and International Potato Center (CIP) sweetpotato breeding programs. Results for plant nematode resistance indicate a bimodal distribution among the genotypes for the LSU population and a normal distribution for the CIP population. Using analysis of molecular variance (AMOVA) at P \u3c 0.001 and two multivariate analysis techniques i.e logistic regression and discriminant analysis, 5 and 4 AFLP markers that had a strong and significant association with respect to the resistance trait were selected for the LSU and CIP populations, respectively. A comparative analysis of the power of discriminant analysis models for southern root-knot nematode resistance class prediction achieved 88.78% (LSU) and 88.04% (CIP) classification efficiencies. © Springer 2005

Impaired Sleep Quality in COPD Is Associated With Exacerbations The CanCOLD Cohort Study

BackgroundCOPD increases susceptibility to sleep disturbances, which may in turn predispose to increased respiratory symptoms. The objective of this study was to evaluate, in a population-based sample, the relationship between subjective sleep quality and risk of COPD exacerbations.MethodsData were obtained from the Canadian Cohort Obstructive Lung Disease (CanCOLD) study. Participants with COPD who had completed 18 months of follow-up were included. Sleep quality was measured with the Pittsburgh Sleep Quality Index (PSQI) and a three-factor analysis. Symptom-based (dyspnea or sputum change ≥ 48 h) and event-based (symptoms plus medication or unscheduled health services use) exacerbations were assessed. Association of PSQI with exacerbation rate was assessed by using negative binomial regression. Exacerbation-free survival was also assessed.ResultsA total of 480 participants with COPD were studied, including 185 with one or more exacerbations during follow-up and 203 with poor baseline sleep quality (PSQI score > 5). Participants with subsequent symptom-based exacerbations had higher median baseline PSQI scores than those without (6.0 [interquartile range, 3.0-8.0] vs 5.0 [interquartile range, 2.0-7.0]; P = .01), and they were more likely to have baseline PSQI scores > 5 (50.3% vs 37.3%; P = .01). Higher PSQI scores were associated with increased symptom-based exacerbation risk (adjusted rate ratio, 1.09; 95% CI, 1.01-1.18; P = .02) and event-based exacerbation risk (adjusted rate ratio, 1.10; 95% CI, 1.00-1.21; P = .048). The association occurred mainly in those with undiagnosed COPD. Strongest associations were with Factor 3 (sleep disturbances and daytime dysfunction). Time to symptom-based exacerbation was shorter in participants with poor sleep quality (adjusted hazard ratio, 1.49; 95% CI, 1.09-2.03).ConclusionsHigher baseline PSQI scores were associated with increased risk of COPD exacerbation over 18 months' prospective follow-up

Impaired Sleep Quality in COPD Is Associated With Exacerbations

BackgroundCOPD increases susceptibility to sleep disturbances, which may in turn predispose to increased respiratory symptoms. The objective of this study was to evaluate, in a population-based sample, the relationship between subjective sleep quality and risk of COPD exacerbations.MethodsData were obtained from the Canadian Cohort Obstructive Lung Disease (CanCOLD) study. Participants with COPD who had completed 18 months of follow-up were included. Sleep quality was measured with the Pittsburgh Sleep Quality Index (PSQI) and a three-factor analysis. Symptom-based (dyspnea or sputum change ≥ 48 h) and event-based (symptoms plus medication or unscheduled health services use) exacerbations were assessed. Association of PSQI with exacerbation rate was assessed by using negative binomial regression. Exacerbation-free survival was also assessed.ResultsA total of 480 participants with COPD were studied, including 185 with one or more exacerbations during follow-up and 203 with poor baseline sleep quality (PSQI score > 5). Participants with subsequent symptom-based exacerbations had higher median baseline PSQI scores than those without (6.0 [interquartile range, 3.0-8.0] vs 5.0 [interquartile range, 2.0-7.0]; P = .01), and they were more likely to have baseline PSQI scores > 5 (50.3% vs 37.3%; P = .01). Higher PSQI scores were associated with increased symptom-based exacerbation risk (adjusted rate ratio, 1.09; 95% CI, 1.01-1.18; P = .02) and event-based exacerbation risk (adjusted rate ratio, 1.10; 95% CI, 1.00-1.21; P = .048). The association occurred mainly in those with undiagnosed COPD. Strongest associations were with Factor 3 (sleep disturbances and daytime dysfunction). Time to symptom-based exacerbation was shorter in participants with poor sleep quality (adjusted hazard ratio, 1.49; 95% CI, 1.09-2.03).ConclusionsHigher baseline PSQI scores were associated with increased risk of COPD exacerbation over 18 months' prospective follow-up