ABSTRACT
Aim: The pathogenic potential of foliar nematode, Aphelenchoides besseyi inducing floral malady symptoms and fluctuation of nematode populations in tuberose were determined under field conditions. Methodology: Pathogenicity of A. besseyi on tuberose cv. Calcutta single was carried out with eight treatments and three replications. The freshly collected A. besseyi was inoculated into tuberose. Observations on plant growth parameters, disease severity and nematode populations were taken and analysed. The population of A. besseyi in tuberose cv. Bidhan Rajani-3 was monitored from the plots of a different set of experiment. Nematode population from flower samples collected from fixed plots at monthly interval during the crop growing period were extracted and estimated. Results: Inoculation of nematodes at higher levels progressively decreased plant growth parameters as compared to uninoculated ones. The inoculated plants displayed typical symptoms of foliar nematode infestation; the outer surface of flower stalk appeared rough, growth stunted, flower stalks distorted, stalk bearing a few florets even failed to bloom. An initial inoculum density of 100 nematodes per plant was found to be pathogenic in tuberose causing significant reduction in yield and quality of flower. Monitoring nematode population during the plant growth period (cv. Bidhan Rajani-3) revealed that A. besseyi maintained maximum population during rainy season coinciding with the start of heavy flush of tuberose and minimum during December to February. Interpretation: An initial inoculum density of 100 A. besseyi per plant was considered pathogenic to tuberose. The nematode population attained peak density during July when the air temperature, relative humidity and total rainfall remained fairly high and lowest during February to December.
ABSTRACT
Aim: The study was conducted to screen the tuberose genotypes for nematode resistance and to establish histopathological, biochemical and nutritional changes in resistant/tolerant genotype against root knot nematode, Meloidogyne incognita. Methodology: Twenty seven tuberose genotypes comprising of two types viz., single (18 genotypes) and double (9 genotypes) were evaluated for root knot nematode resistance. Tuberose bulbs of uniform size were surface sterilized and planted in 9 inch plastic pots and inoculated with nematode juveniles (J2) 15 days after planting. Gall Index was recorded on a 0-5 scale after 120 days of inoculation. Histopathological, biochemical (total phenols, peroxidase, polyphenol oxidase and phenylalanine ammonia lyase) and nutrient estimation studies were conducted on the roots of resistant/tolerant genotypes against root knot nematode, Meloidogyne incognita. Results: Among the twenty seven tuberose genotypes screened for nematode resistance, Suarna Rekha was categorized as resistant genotype and Arka Shirngar, IIHR-2, IIHR-4, Variegated, IIHR-12, GK-T-C4, Calcutta Double, Bidhan Rajani-2 and Bidhan Rajani-3 were categorized as tolerant genotypes. Histological characterization of resistant/tolerant genotypes revealed that giant cell formation was disrupted with higher number of phenolic cells and cells with lignified cell wall that prevented the successful establishment of nematode feeding site. The resistant and tolerant genotypes significantly recorded higher accumulation of phenols and defence enzymes viz., polyphenol oxidase (PPO), peroxidase (PO) and phenyl alanine ammonia lyase (PAL) and macro and micro nutrients as compared to susceptible genotypes. Interpretation: Screening of tuberose genotypes for root knot nematode resistance in this study has led to the identification of several nematode resistant/ tolerant genotypes. This would serve as a valuable information for the breeders to utilize resistant/ tolerant genotypes as parents in their breeding programmes.
ABSTRACT
El Complejo Esclerosis Tuberosa (CET) es una enfermedad de origen genético, multisistémica de transmisión autosómica dominante, se debe a la mutación de los genes TSC1 (Tuberose Sclerosis Complex 1) y TSC2 de los cromosomas 9 y 16 respectivamente. Las manifestaciones clínicas se deben a la presencia de lesiones tumorales benignas (harmatomas) en diferentes órganos lo que genera un amplio espectro de signos y síntomas. El caso que se presenta es de una adolescente de origen aymara con epilepsia, retraso mental y lesiones dérmicas típicas. Es una enfermedad poco frecuente en nuestro medio y rara en personas de origen indígena, no encontrándose ninguna descripción en la literatura nacional. Por la multiplicidad de las manifestaciones clínicas, se hace necesario divulgar la información para que que las diferentes especialidades médicas reconozcan y diagnostiquen esta patología tempranamente para un tratamiento adecuado, oportuno y interdisciplinar.
The Tuberose Sclerosis Complex (TSC) is a genetic, multisystemic disease of autosomal dominant transmission, due to the mutation of the TSC1 and TSC2 genes of chromosomes 9 and 16 respectively. The clinical manifestations are due to the presence of benign tumor lesions (harmatomas) in different organs, which generates a wide spectrum of signs and symptoms. The case presented is that of a teenager of Aymara origin with epilepsy, mental retardation and typical skin lesions. It is a rare disease in our environment and rare in people of indigenous origin, no description found in the national literature. Due to the multiplicity of the clinical manifestations, it is necessary to disseminate the information so that the different medical specialties recognize and diagnose this pathology early for an adequate, timely and interdisciplinary treatment.