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32.
Effect of abscisic acid application on root isoflavonoid concentration and nodulation of wild-type and nodulation-mutant soybean plants 总被引:1,自引:0,他引:1
Isoflavonoids (daidzein, genistein, and coumestrol) are involved in induction of nod genes in Bradyrhizobium japonicum and may be involved in nodule development as well. Abscisic acid (ABA) may also impact nodulation since ABA is reportedly
involved in isoflavonoid synthesis. The current study was conducted to evaluate whether ABA plays a role in differential nodulation
of a hypernodulated soybean (Glycine max L. Merr.) mutant and the Williams parent. Exogenous ABA application resulted in a decrease in nodule number and weight in
both lines. Isoflavonoid concentrations were also markedly decreased in response to ABA application in both inoculated and
noninoculated soybean roots. The inoculation treatment itself resulted in a marked increase in isoflavonoid concentrations
of NOD1-3, regardless of ABA levels, while only slight increases occurred in Williams. The nodule numbers of both soybean
lines across several ABA concentration treatments were highly correlated with the concentration of all three isoflavonoids.
However, differences in internal levels of ABA between lines were not detected when grown in the absence of external ABA additions.
It is concluded that differential nodule expression between the wild type and the hypernodulated mutant is not likely due
to differential ABA synthesis. 相似文献
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Hai B. Tran Suzanne Maiolo Rebecca Harper Peter D. Zalewski Paul N. Reynolds Sandra Hodge 《Cell biology international》2021,45(11):2368-2379
Recently identified molecular targets in pulmonary artery hypertension (PAH) include sphingosine-1-phosphate (S1P) and zinc transporter ZIP12 signaling. This study sought to determine linkages between these pathways, and with BMPR2 signaling. Lung tissues from a rat model of monocrotaline-induced PAH and therapeutic treatment with bone marrow–derived endothelial-like progenitor cells transduced to overexpress BMPR2 were studied. Multifluorescence quantitative confocal microscopy (MQCM) was applied for analysis of protein expression and localization of markers of vascular remodeling (αSMA and BMPR2), parameters of zinc homeostasis (zinc transporter SLC39A/ZIP family members 1, 10, 12 and 14; and metallothionein MT3) and S1P extracellular signaling (SPHK1, SPNS2, S1P receptor isoforms 1, 2, 3, 5) in 20–200 µm pulmonary microvessels. ZIP12 expression in whole lung tissue lysates was assessed by western blot. Spearman nonparametric correlations between MQCM readouts and hemodynamic parameters, Fulton index (FI), and right ventricular systolic pressure (RVSP) were measured. In line with PAH status, pulmonary microvessels in monocrotaline-treated animals demonstrated significant (p < .05, n = 6 per group) upregulation of αSMA (twofold) and downregulation of BMPR2 (20%). Upregulated ZIP12 (92%), MT3 (57.7%), S1PR2 (54.8%), and S1PR3 (30.3%) were also observed. Significant positive and negative correlations were demonstrated between parameters of zinc homeostasis (ZIP12, MT3), S1P signaling (S1PRs, SPNS2), and vascular remodeling (αSMA, FI, RVSP). MQCM and western blot analysis showed that monocrotaline-induced ZIP12 upregulation could be partially negated by BMPR2-targeted therapy. Our results indicate that altered zinc transport/storage and S1P signaling in the monocrotaline-induced PAH rat model are linked to each other, and could be alleviated by BMPR2-targeted therapy. 相似文献
35.
Keloid fibroblasts in culture: abnormal growth behaviour and altered response to the epidermal growth factor 总被引:1,自引:0,他引:1
R A Harper 《Cell biology international reports》1989,13(4):325-335
Keloid fibroblasts were propagated in culture and their proliferative behaviour and response to the Epidermal Growth Factor (EGF) were studied. Keloid fibroblasts grew at a rate which was approximately one-half that of normal age, sex and race matched control fibroblasts. Keloid fibroblasts were stimulated to grow in the presence of EGF (10 ng/ml), but to a lesser degree than the normal control fibroblasts. Scatchard analysis of the binding data obtained using 125I-labeled EGF revealed no difference in binding affinity or receptor numbers between keloid and normal fibroblasts. 相似文献
36.
Localization of a human Na+,K+-ATPase alpha subunit gene to chromosome 19q12----q13.2 and linkage to the myotonic dystrophy locus 总被引:3,自引:0,他引:3
H G Harley J D Brook C L Jackson T Glaser K V Walsh M Sarfarazi R Kent M Lager M Koch P S Harper 《Genomics》1988,3(4):380-384
The gene coding for a Na+,K+-ATPase alpha subunit (ATP1A3) has been localized to the q12----q13.2 region of human chromosome 19, potentially close to the myotonic dystrophy (DM) gene. In view of previous studies implicating a Na+,K+-ATPase in the pathology of DM, we have examined the possibility that ATP1A3 is a candidate for the DM locus. Although linked, several clear instances of recombination between ATP1A3 and DM rule out the possibility that mutations in ATP1A3 cause the disease. Examination of multiply informative pedigrees indicates the gene order DM-APOC2-ATP1A3. 相似文献
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