Morphological Markers based Assessment of Genetic Diversity in Cultivated Tomato (Solanum Lycopersicon L.) Genotypes

Assessment of genetic diversity in any crop species provides a basis for devising future strategies for crop improvement; conservation and sustainable use. An experiment consisting of 24 genotypes of Tomato was conducted during the year 2016 at the Research Farm and Molecular Biology Laboratory of School of Biotechnology, SKUAST-J, Chatha. The experiment was conducted in Randomised Block Design (RBD) with three replications in 2 rows of 5m length with spacing of 45 x 90 cm. The extent of genetic divergence /relatedness was estimated among 24 genotypes by using 11 traits viz. plant height (cm), number of branches, number of fruits per bunch, total soluble solids, flesh thickness (mm), number of locules, fruit width (cm), fruit length (cm), yield per plant (g), average fruit weight (g), number of fruits per plant. The maximum number of fruits/bunch was recorded in “Utkal Pragyan” (3.66) and the minimum number was recorded in “Swarna Sampada” (2.03). Maximum TSS(%) was recorded in DCT-1 (8.06%) and minimum TSS was recorded in “Dhanshri” (2.83%). Maximum number of fruits and yield/plant was recorded in “DCT-1” (115.33) and “Hisar Lalit” (2507.36g), respectively. The minimum number of fruits and yield/ plant was recorded in “NDT-4” (23.20) and “DCT-1” (861.40g), respectively.Mean data revealed high range for most of studied traits. Hierarchical cluster analysis allowed the assessment of similarity and clarified some of the relationships among tomato genotypes. UPGMA produced a dendrogram with two main clusters with further sub clusters. Of all the studied 24 genotypes Anand tomato and Hisar lalit were found to be most dissimilar based on UPGMA clustering. Hisar lalit was found to be most promising variety among all the genotypes for most of the traits under study, which can be used for further breeding and crop improvement programmes

Efficacy of antimicrobial treatment in non-dysenteric persistent diarrhoea in a community setting

To determine the efficacy of antimicrobial treatment in non-dysenteric persistent diarrhoea in a community setting. In this double-blind field trial, 156 children aged 4-36 months with persistent diarrhoea not associated with Giardia lamblia infestation seeking treatment in a community outpatient clinic, were randomized to receive a combination of nalidixic acid and metronidazole, metronidazole alone, or placebo for 7 days. In comparison with placebo, metronidazole treatment did not result in a significant reduction in the mean post-enrollment diarrhoeal duration and stool frequency, increase in the proportion of patients recovered by days 3, 5 and 7 of treatment, and increase in weight gain at days 7 and 14. Comparing the combination of nalidixic acid and metronidazole with metronidazole alone, 17.5% more children treated with the combination recovered by day 3 of treatment (p = 0.08) and the mean stool frequency ascertained on day 7 for the previous 24 h was 26.8% less in them (p = 0.05). The weight gains at days 7 and 14 were similar in the two groups. These findings indicate that metronidazole offers no therapeutic benefit in persistent diarrhoea not associated with Giardia lamblia and nalidixic acid has only a modest clinical benefit, which is not substantial enough to warrant its routine use

XBP1-KLF9 Axis Acts as a Molecular Rheostat to Control the Transition from Adaptive to Cytotoxic Unfolded Protein Response

Summary: Transcription factor XBP1s, activated by endoplasmic reticulum (ER) stress in a dose-dependent manner, plays a central role in adaptive unfolded protein response (UPR) via direct activation of multiple genes controlling protein refolding. Here, we report that elevation of ER stress above a critical threshold causes accumulation of XBP1s protein sufficient for binding to the promoter and activation of a gene encoding a transcription factor KLF9. In comparison to other XBP1s targets, KLF9 promoter contains an evolutionary conserved lower-affinity binding site that requires higher amounts of XBP1s for activation. In turn, KLF9 induces expression of two regulators of ER calcium storage, TMEM38B and ITPR1, facilitating additional calcium release from ER, exacerbation of ER stress, and cell death. Accordingly, Klf9 deficiency attenuates tunicamycin-induced ER stress in mouse liver. These data reveal a role for XBP1s in cytotoxic UPR and provide insights into mechanisms of life-or-death decisions in cells under ER stress. : The transcription factor XBP1s plays a central role in suppression of endoplasmic reticulum (ER) stress through direct activation of multiple genes controlling protein refolding. Fink et al. report that elevation of ER stress above a certain threshold triggers an XBP1s-dependent transcriptional program, leading to exacerbation of ER stress and cell death. Keywords: endoplasmic reticulum stress, XBP1s, KLF9, TMEM38B, ITPR1, calcium channel, UP

A Purine Nucleotide Biosynthesis Enzyme Guanosine Monophosphate Reductase Is a Suppressor of Melanoma Invasion

Melanoma is one of the most aggressive types of human cancers, and the mechanisms underlying melanoma invasive phenotype are not completely understood. Here, we report that expression of guanosine monophosphate reductase (GMPR), an enzyme involved in de novo biosynthesis of purine nucleotides, was downregulated in the invasive stages of human melanoma. Loss- and gain-of-function experiments revealed that GMPR downregulates the amounts of several GTP-bound (active) Rho-GTPases and suppresses the ability of melanoma cells to form invadopodia, degrade extracellular matrix, invade in vitro, and grow as tumor xenografts in vivo. Mechanistically, we demonstrated that GMPR partially depletes intracellular GTP pools. Pharmacological inhibition of de novo GTP biosynthesis suppressed whereas addition of exogenous guanosine increased invasion of melanoma cells as well as cells from other cancer types. Our data identify GMPR as a melanoma invasion suppressor and establish a link between guanosine metabolism and Rho-GTPase-dependent melanoma cell invasion