Downregulation of miR-135b-5p Suppresses Progression of Esophageal Cancer and Contributes to the Effect of Cisplatin

Esophageal cancer (EC) is one of the commonest human cancers, which accompany high morbidity. MicroRNAs (miRNAs) play a pivotal role in various cancers, including EC. Our research aimed to reveal the function and mechanism of miR-135b-5p. Our research identified that miR-135b-5p was elevated in EC samples from TCGA database. Correspondingly real-time PCR assay also showed the miR-135b-5p is also higher expressed in Eca109, EC9706, KYSE150 cells than normal esophageal epithelial cells (Het-1A). CCK8, Edu, wound healing, Transwell assay, and western blot demonstrated miR-135b-5p inhibition suppresses proliferation, invasion, migration and promoted the apoptosis in Eca109 and EC9706 cells. Moreover, the miR-135b-5p inhibition also inhibited xenograft lump growth. We then predicted the complementary gene of miR-135b-5p using miRTarBase, TargetScan, and DIANA-microT. TXNIP was estimated as a complementary gene for miR-135b-5p. Luciferase report assay verified the direct binding site for miR-135b-5p and TXNIP. Real-time PCR and western blot assays showed that the inhibition of miR-135b-5p remarkably enhanced the levels of TXNIP in Eca109 and EC9706 cells. Furthermore, cisplatin (cis-diamminedichloroplatinum II, DDP) decreased miR-135b-5p expression and increased TXNIP expression. Enhanced expression of miR-135b-5p attenuated the inhibitory ability of cisplatin (cis-diamminedichloroplatinum II, DDP) in Eca109 cells, accompanied by TXNIP downregulation. In conclusion, the downregulation of miR-135b-5p suppresses the progression of EC through targeting TXNIP. MiR-135b-5p/TXNIP pathway contributes to the anti-tumor effect of DDP. These findings may provide new insight into the treatment of EC.

Inheritance Pattern of Mungbean Yellow Mosaic Virus (MYMV) Disease Resistance in Blackgram [Vigna mungo (L.) Hepper]

Background: Mungbean yellow mosaic virus (MYMV) disease is the most destructive disease in blackgram. Development of MYMV resistant varieties is one of the best possible solutions to avoid the yield reduction in blackgram. There are conflicting reports on the genetics of resistance to MYMV disease claiming that it is controlled by both dominant and recessive genes. Hence the present study was aimed to understand the inheritance pattern of the MYMV disease resistance in eight crosses of blackgram.Methods: Parents, F1 and F2 generation of eight cross combinations were raised during July - Sep, 2018 at National Pulses Research Centre, Tamil Nadu Agricultural University, Vamban, Tamil Nadu. An infector row of CO 5 was raised to intensify the MYMV disease pressure after every eight rows. Based on disease incidence on 60th day after sowing, two phenotypic classes were formed among F2 plants with the scales of (1 to 3) as resistant phenotype and (4 to 9) as susceptible phenotype. The goodness of fit to Mendelian segregation ratio for MYMV disease resistance in the segregating population was tested by Chi square test (Stansfield, 1991).Result: The MYMV disease incidence was tri-genically controlled with inhibitory gene action in four crosses viz., MDU 1 x Mash 114, CO5 x Mash 114, MDU 1 x VBN 6 and CO 5 x VBN 6. Complementary gene action with two genes was observed in four crosses viz., MDU 1 x Mash 1008, CO 5 x Mash 1008, MDU 1 x VBN 8 and CO 5 x VBN 8. Differences in number of genes were observed due to the presence of recessive inhibitory gene in both male and female parents of the crosses which had complementary gene action for MYMV disease. The putative gene symbols assigned for the six genotypes viz., S1S1S2S2ii (MDU 1 and CO 5), s1s1s2s2II (Mash 114 and VBN 6) and s1s1s2s2ii (Mash 1008 and VBN 8), respectively.

Genetic analysis of various quantitative traits ininter-varietal crosses of Vigna mungo

Gene effects for 13 characters in four crosses of Vigna mungo were studied by six parameter generation mean model to determine the potential for the improvement of yield components. Scaling tests revealed inadequacy of the additive-dominance model for all the traits indicating the presence of non-allelic interactions. Duplicate gene action was observed for six characters in KUG-216 x HPBU-111, five in KUG-216 x Palampur-93, two in IPU-05-13 x Palampur-93 and one in IPU-05-13 x HPBU-111 and complementary gene action for one character each in KUG-216 x Palampur-93 and IPU-05-13 x HPBU-111 cross. Selection in later generations for duplicate gene action and early generation selection involving intermatings in F2 f or complementary gene action should be adopted for harnessing desirable recombinants.

Genetic Analysis of the Resistance to Eight Anthracnose Races in the Common Bean Differential Cultivar Kaboon

Resistance to the eight races (3, 7, 19, 31, 81, 449, 453, and 1545) of the pathogenic fungus Colletotrichum lindemuthianum (anthracnose) was evaluated in F3 families derived from the cross between the anthracnose differential bean cultivars Kaboon and Michelite. Molecular marker analyses were carried out in the F2 individuals in order to map and characterize the anthracnose resistance genes or gene clusters present in Kaboon. The analysis of the combined segregations indicates that the resistance present in Kaboon against these eight anthracnose races is determined by 13 different race-specific genes grouped in three clusters. One of these clusters, corresponding to locus Co-1 in linkage group (LG) 1, carries two dominant genes conferring specific resistance to races 81 and 1545, respectively, and a gene necessary (dominant complementary gene) for the specific resistance to race 31. A second cluster, corresponding to locus Co-3/9 in LG 4, carries six dominant genes conferring specific resistance to races 3, 7, 19, 449, 453, and 1545, respectively, and the second dominant complementary gene for the specific resistance to race 31. A third cluster of unknown location carries three dominant genes conferring specific resistance to races 449, 453, and 1545, respectively. This is the first time that two anthracnose resistance genes with a complementary mode of action have been mapped in common bean and their relationship with previously known Co- resistance genes established.