Pengimbasan Ketahanan Pisang terhadap Penyakit Layu Fusarium dengan Asam Salisilat In Vitro

Salicylic acid (SA) is an important signal in plant defense. It is used as induced resistance agent against Fusarium wilt. An artificial induction was conducted by shaking the shoot groups of banana tissue culture in liquid medium of Murashige-Skoog (MS). MS medium was added with 0 ppm (as control), ⅛ LC50, ¼ LC50, ½ LC50, and LC50 concentration of SA. Alive shoot groups were subcultured for about three months and were acclimated. Resistance test had been conducted in glass house by inoculated six months old banana seedlings with Fusarium oxysporum f.sp. cubense (Foc). Leaves symptom were observed based on Leaf Symptom Index (LSI) and corm discoloration based on Rhizome Discoloration Index (RDI). The result of this research showed that induced banana seedlings had higher plant resistance to Fusarium wilt than control. Asam salisilat (SA) merupakan signal penting dalam ketahanan tanaman, digunakan sebagaisenyawa pengimbas ketahanan tanaman pisang terhadap penyakit layu Fusarium. Pengimbasan dilakukan pada kelompok tunas kultur jaringan pisang dalam medium kultur jaringan MS cair dengan konsentrasi SA 0 ppm (sebagai kontrol), ⅛ LC50, ¼ LC50,½LC50 danLC50.Tunas yang bertahan hidup ditumbuhkan sebagai bibit dan uji ketahanan dilakukan dirumah kaca dengan inokulasiFusariumoxysporumf.sp. cubense (Foc) pada bibit pisang umur enambulan pasca aklimatisasi. Pengamatan dilakukan terhadap gejala layu pada daun (Leaf Symptom Index = LSI) dan diskolorasi pada bonggol (Rhizome Discoloration Index=RDI). Hasil penelitianmenunjukkan bahwa bibit pisang hasil pengimbasanmemiliki ketahanan yang lebih tinggi dibandingkan dengan perlakuan kontrol

An Empirical Validation Of The Primary And Moderating Effects Of Income And Capital On Familiarity And Participation Of Limited Resource Farm Producers (LRFPs) In USDA Agricultural Programs

We present empirical findings on the problem of low participation rate of Limited Resource Farm Producers (LRFPs)[1] in USDA programs. Our analysis is based on survey data directly sourced from LRFP population spread across twenty counties in Southern Virginia. The findings revealed that familiarity with and participation in USDA programs varied by type of farmers. While familiarity was moderate, participation was low. These main effects were moderated by access to capital. Our results broadly agree with findings from similar studies done on the subject in the past with an additional empirical insight that access to capital can enhance participation in USDA programs. We conclude the study with several practical ways for improving LRFP participation in USDA agricultural programs[i] According to the USDA, a Limited Resource Farmer or Rancher or Forest Owner is a person/applicant with direct or indirect gross farm sales not more than $173,600 (for FY2016) in each of the previous two years AND a person with a total household income at or below the national poverty level for a family of four or less than 50 percent of county median household income in each of the previous two years. An entity or joint operation can be an LRFP if all individual members independently qualify. http://lrftool.sc.egov.usda.gov/LRP_Definition.aspx http://www.nrcs.usda.gov/wps/portal/nrcs/main/national/people/outreach/slbfr

Deteksi Pengimbasan Ketahanan Pisang terhadap Penyakit Layu Fusarium dengan Asam Fusarat

Fusarium wilt caused by Fusarium oxysporum f. sp. cubense (Foc) is the most destructive disease of banana. Until today this disease has not been successfully controlled. Fusaric acid is a toxin produced by Foc. Tyloses produced in xylem that caused wilting and yellowing of banana plants, inhibit soil nutrition and water stream. The study carried out previously showed that enriched fusaric acid in banana culture induced the resistance of banana seedlings against Foc. The signal of induced resistance increased the phenolic compounds. One of the phenolic compounds is salicylic acid. The aim of this study was to detect induced resistance of banana plant from tissue cultured enriched with fusaric acid. The experiment was done in the field highly infected with Foc. Observation of resistance was done by measuring disease percentage of yellowing and wilting leaves.Tyloses produced in xylem was observed microscopically from cross section of root. Root damage intensity was counted using tyloses score. Salicylic acid content of root was analyzed with phenolic compounds method using HPLC. The results showed that banana plants from enriched tissues culture with 1.165 ppm of fusaric acid increased the resistance against Foc, but salicylic acid was not detected. Salicylic acid was only detected at low concentration (2 ppb) in moderate resistant banana roots from induced plants with 9.32 ppm of fusaric acid. The chromatogram showed three peaks of unknown phenolic compounds. Tyloses intensity was not related with induced resistance of banana against fusarium wilt. Advanced research is needed with more plants samples. It was suggested to identify the phenolic compounds which were detected in induced resistant plant.INTISARILayu fusarium yang disebabkan oleh Fusarium oxysporum f. sp. cubense (Foc) adalah penyakit yang sangat merusak pada pisang dan belum dapat dikendalikan secara tuntas. Gejala berupa kelayuan daun karena tersumbatnya xilem karena pembentukan tilosis yaitu pertumbuhan sel dalam jaringan xilem. Pengimbasan ketahanan diharapkan dapat menjadi salah satu cara pengendalian penyakit layu fusarium. Penelitian sebelumnya menunjukkan penambahan asam fusarat dalam kultur jaringan dapat mengimbas ketahanan bibit pisang terhadap penyakit layu fusarium. Asam salisilat adalah salah satu signal ketahanan yang akan meningkat kandungannya bila terjadi peningkatan ketahanan akibat pengimbasan. Penelitian ini bertujuan untuk mendeteksi hasil pengimbasan ketahanan pisang dengan asam fusarat dalam kultur jaringan. Tanaman telah ditanam di lapangan yang terinfeksi berat oleh Foc. Intensitas penyakit di lapang diamati dengan menghitung persentase daun menguning dan atau layu. Intensitas kerusakan akar diamati dengan pembuatan irisan tipis dan pengamatan tilosis dengan cara skoring. Analisis asam salisilat dalam akar dilakukan dengan metode analisis senyawa fenol menggunakan HPLC. Hasil penelitian tanaman dari bibit yang diimbas dengan 1,165 ppm asam fusarat dalam kultur jaringan menunjukkan peningkatan ketahanan di lapang. Intensitas tilosis lebih rendah pada tanaman yang diimbas ketahanannya dibandingkan yang tidak diimbas. Asam salisilat dalam tanaman yang diimbas ketahannnya denga asam fusarat 9,32 ppm terdeteksi pada konsentrasi yang sangat rendah yaitu 2 ppb, dengan ketahanan moderat. Pada tanaman hasil pengimbasan yang menunjukkan kriteria tahan asam salisilat tidak terdeteksi, namun terdeteksi tiga puncak senyawa fenol yang belum teridentifikasi. Intensitas tilosis pada tanaman yang diimbas ketahanannya tidak menunjukkan penurunan dibandingkan dengan tanaman yang tidak diperlakukan. Penelitian ini perlu dilanjutkan dengan sampel yang lebih banyak. Identifikasi jenis senyawa fenol perlu dilakukan dalam penelitian lanjutan

Metabolic Control Analysis in a Cellular Model of Elevated MAO-B: Relevance to Parkinson’s Disease

We previously demonstrated that spare respiratory capacity of the TCA cycle enzyme alpha-ketoglutarate dehydrogenase (KGDH) was completely abolished upon increasing levels of MAO-B activity in a dopaminergic cell model system (Kumar et al., J Biol Chem 278:46432–46439, 2003). MAO-B mediated increases in H2O2 also appeared to result in direct oxidative inhibition of both mitochondrial complex I and aconitase. In order to elucidate the contribution that each of these components exerts over metabolic respiratory control as well as the impact of MAO-B elevation on their spare respiratory capacities, we performed metabolic respiratory control analysis. In addition to KGDH, we assessed the activities and substrate-mediated respiration of complex I, pyruvate dehydrogenase (PDH), succinate dehydrogenase (SDH), and mitochondrial aconitase in the absence and presence of complex-specific inhibitors in specific and mixed substrate conditions in mitochondria from our MAO-B elevated cells versus controls. Data from this study indicates that Complex I and KGDH are the most sensitive to inhibition by MAO-B mediated H2O2 generation, and could be instrumental in determining the fate of mitochondrial metabolism in this cellular PD model system

Bioactivity, biocompatibility and antimicrobial properties of a chitosan-mineral composite for periodontal tissue regeneration

A composite membrane of the polymer, chitosan, and the silver-exchanged mineral phase, tobermorite, was prepared by solvent casting and characterised by scanning electron microscopy and Fourier transform infrared spectroscopy. The in vitro bioactivity, cytocompatibility and antimicrobial activity of the composite were evaluated with respect to its potential application as a guided tissue regeneration (GTR) membrane. The in vitro bioactivity was verified by the formation of hydroxyapatite on the surface of the membrane in simulated body fluid and its cytocompatibility was established using MG63 human osteosarcoma cells. The presence of silver ions conferred significant antimicrobial activity against S. aureus, P. aeruginosa and E. coli. The findings of this investigation have indicated that the chitosansilver-tobermorite composite is a prospective candidate for GTR applications

PINK1 Is Necessary for Long Term Survival and Mitochondrial Function in Human Dopaminergic Neurons

Parkinson's disease (PD) is a common age-related neurodegenerative disease and it is critical to develop models which recapitulate the pathogenic process including the effect of the ageing process. Although the pathogenesis of sporadic PD is unknown, the identification of the mendelian genetic factor PINK1 has provided new mechanistic insights. In order to investigate the role of PINK1 in Parkinson's disease, we studied PINK1 loss of function in human and primary mouse neurons. Using RNAi, we created stable PINK1 knockdown in human dopaminergic neurons differentiated from foetal ventral mesencephalon stem cells, as well as in an immortalised human neuroblastoma cell line. We sought to validate our findings in primary neurons derived from a transgenic PINK1 knockout mouse. For the first time we demonstrate an age dependent neurodegenerative phenotype in human and mouse neurons. PINK1 deficiency leads to reduced long-term viability in human neurons, which die via the mitochondrial apoptosis pathway. Human neurons lacking PINK1 demonstrate features of marked oxidative stress with widespread mitochondrial dysfunction and abnormal mitochondrial morphology. We report that PINK1 plays a neuroprotective role in the mitochondria of mammalian neurons, especially against stress such as staurosporine. In addition we provide evidence that cellular compensatory mechanisms such as mitochondrial biogenesis and upregulation of lysosomal degradation pathways occur in PINK1 deficiency. The phenotypic effects of PINK1 loss-of-function described here in mammalian neurons provides mechanistic insight into the age-related degeneration of nigral dopaminergic neurons seen in PD

Impaired mitochondrial biogenesis contributes to depletion of functional mitochondria in chronic MPP+ toxicity: dual roles for ERK1/2

The regulation of mitochondrial quality has emerged as a central issue in neurodegeneration, diabetes, and cancer. We utilized repeated low-dose applications of the complex I inhibitor 1-methyl-4-phenylpyridinium (MPP+) over 2 weeks to study cellular responses to chronic mitochondrial stress. Chronic MPP+ triggered depletion of functional mitochondria resulting in diminished capacities for aerobic respiration. Inhibiting autophagy/mitophagy only partially restored mitochondrial content. In contrast, inhibiting activation of extracellular signal-regulated protein kinases conferred complete cytoprotection with full restoration of mitochondrial functional and morphological parameters, enhancing spare respiratory capacity in MPP+ co-treated cells above that of control cells. Reversal of mitochondrial injury occurred when U0126 was added 1 week after MPP+, implicating enhanced repair mechanisms. Chronic MPP+ caused a >90% decrease in complex I subunits, along with decreases in complex III and IV subunits. Decreases in respiratory complex subunits were reversed by co-treatment with U0126, ERK1/2 RNAi or transfection of dominant-negative MEK1, but only partially restored by degradation inhibitors. Chronic MPP+ also suppressed the de novo synthesis of mitochondrial DNA-encoded proteins, accompanied by decreased expression of the mitochondrial transcription factor TFAM. U0126 completely reversed each of these deficits in mitochondrial translation and protein expression. These data indicate a key, limiting role for mitochondrial biogenesis in determining the outcome of injuries associated with elevated mitophagy