In the mouse, the process of implantation is initiated by the attachment reaction between the blastocyst trophectoderm and uterine luminal epithelium that occurs at 2200-2300 h on day 4 (day 1 = vaginal plug) of pregnancy. Several members of the EGF family are considered important in embryo-uterine interactions during implantation. This investigation demonstrates that the expression of two additions to the family, betacellulin and epiregulin, are exquisitely restricted to the mouse uterine luminal epithelium and underlying stroma adjacent to the implanting blastocyst. These genes are not expressed during progesterone-maintained delayed implantation, but are rapidly switched on in the uterus surrounding the implanting blastocyst following termination of the delay by estrogen. These results provide evidence that expression of betacellulin and epiregulin in the uterus requires the presence of an active blastocyst and suggest an involvement of these growth factors in the process of implantation.
Susceptibility to root-knot nematodes (Meloidogyne spp.) is one of the major factors limiting mungbean production in South and South-east Asia. Host-pest-environment interaction in mungbean and rootknot nematode (M. incognita) was investigated in multi-location field evaluation using 38 promising mungbean genotypes extracted from initial evaluation of 250 genotypes under sick plots considering second stage freshly hatched juvenile as inoculants. the extent of environmental and genotypeby-environment interactions (GGe) was assessed to comprehend the dynamism of resistance and identification of durable resistant mungbean genotypes. Among environmental factors, nematode activity was highly influenced by rainfall and minimum temperature. The GGE biplot and multiple comparison tests detected a higher proportion of genotype × environment (Ge) interaction followed by genotype and environment on number of nematode galls, gall index and reproduction factor. The first two principal components (PCs) explained 64.33% and 66.99% of the total variation of the environment-centered gall scoring and reproduction factor data, respectively. the high Ge variation indicated the presence of non-cross over interactions which justify the necessities of multi-location testing. Detection of non-redundant testing locations would expedite optimum resource utilization in future. The GGE biplot analysis identified genotypes such as PM-10-12, IPM-410-3 and NVL-641 as the outperforming and desirable genotypes with durable resistance against M. incognita which can be exploited in mungbean breeding programmes globally. on the contrary, the highest gall scoring and reproduction factor were recorded in genotype IPM-9901-8. Computation of confidence interval (CI) at 95% level through bootstrapping increased precision of GGE biplot towards genotype recommendation. furthermore, total phenol content, ascorbic acid, phenlylalanine ammonia lyase (pAL) and polyphenol oxidase (PPO) activities were also higher in identified resistant genotypes and this information would be useful for devising mungbean breeding strategies in future for resistance against root-knot nematodes.Mungbean (Vigna radiata L.Wilczek) is an important nutritious pulse crop playing a crucial role in combating malnutrition among vegetarian population of South and South-East Asia (SEA), Africa, South America and Australia 1 . Notwithstanding, the increase in area and production, productivity of this crop is quite low as compared to other pulse crops 2 . There are several biotic and abiotic stresses including root-knot nematodes which are responsible for low productivity of mungbean 3,4 . Root-knot nematodes (Meloidogyne spp.) mainly affect mungbean production in South, East, and Southeast Asia, Africa and South America 5 and cause 18-90 percent yield damage in congenial conditions 4,6-8 . These are serious parasites which attack wide varieties of crop plants including pulses and are responsible for substantial economic losses 9 . M. incognita is widely distributed and pest of several econ...
Earlier, we reported that the bacteriophage lambda P gene product is lethal to Escherichia coli, and the E. coli rpl mutants are resistant to this lambda P gene-mediated lethality. In this paper, we show that under the lambda P gene-mediated lethal condition, the host DNA synthesis is inhibited at the initiation step. The rpl8 mutation maps around the 83 min position in the E. coli chromosome and is 94 % linked with the dnaA gene. The rpl8 mutant gene has been cloned in a plasmid. This plasmid clone can protect the wild-type E. coli from lambda P gene-mediated killing and complements E. coli dnaAts46 at 42 degrees C. Also, starting with the wild-type dnaA gene in a plasmid, the rpl-like mutations have been isolated by in vitro mutagenesis. DNA sequencing data show that each of the rpl8, rpl12 and rpl14 mutations has changed a single base in the dnaA gene, which translates into the amino acid changes N313T, Y200N, and S246T respectively within the DnaA protein. These results have led us to conclude that the rpl mutations, which make E. coli resistant to lambda P gene-mediated host lethality, are located within the DNA initiator gene dnaA of the host.
Cell-cell interactions between the blastocyst trophectoderm and uterine luminal epithelium are essential to the process of implantation. The factors that participate in these interactions or their mechanism of actions are poorly understood. Histamine has long been suspected as one of the factors that is involved in implantation. Histamine is formed from L-histidine by histidine decarboxylase (HDC). We examined the expression and regulation of HDC gene in the mouse uterus during early pregnancy and under steroid hormonal stimulation. Northern blot hybridization detected a 2.6-kb transcript of HDC messenger RNA (mRNA) in uterine poly(A)+ RNA samples. Maximum uterine accumulation of HDC mRNA occurred on days 3 and 4 of pregnancy, followed by marked declines on later days (days 5-8). In ovariectomized mice, uterine mRNA levels were up-regulated by an injection of progesterone (P4) by 6 h, and the levels were maintained through 24 h. In contrast, an injection of estradiol-17beta neither stimulated nor antagonized P4-induced HDC mRNA accumulation. P4-induced up-regulation was considerably abrogated by pretreatment with RU-486, a P4 receptor antagonist, suggesting involvement of P4 receptor. In situ hybridization detected HDC mRNA specifically in uterine epithelial cells but not in other cell types. Again, high epithelial accumulation occurred on day 4 of pregnancy. With the progression of implantation (days 5-8), HDC mRNA levels declined in the luminal epithelium surrounding the implanting blastocysts, as compared with that away from the blastocysts. Immunoreactive histamine and HDC were colocalized with HDC mRNA. Western blotting detected a 54-kDa protein in epithelial cell extracts, which also exhibited HDC activity. Expression of HDC in epithelial cells, preceding implantation on day 4, at lower levels after initiation of implantation on day 5, and its regulation by P4 suggest that this gene plays an important role in implantation.
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