S-allele-specific proteins (S-proteins) were separated and identified by two-dimensional (2D) gel electrophoresis from the style extract of 14 cultivars of Japanese pear, Pyrus pyrifolia Nakai, which exhibits gametophytic self-incompatibility. These S-proteins were 30-32 kDa basic proteins with putative pIs of 9.6-10.1 and were distinct from the other proteins, which were common for all cultivars examined. Each S-protein was assigned to a given S-genotype based on electrophoretic mobility and the partial amino acid sequence. For S1- to S7-proteins, five different N-terminal amino acid sequences sharing the YFQFTQQY sequence were determined. Since the same N-terminal amino acid sequences were found for both S1- and S7-proteins, and for S3- and S5-proteins, the two S-proteins of each pair were distinguished based on their electrophoretic behavior. The internal amino acid sequences of S2- and S4-proteins, determined for Achromobacter protease I (API) digests, revealed that these proteins are S2- and S4-RNases, respectively. In the cultivar Nijisseiki, these two RNases were expressed from the white bud to mature flower stages when the cultivar acquires and enforces self-incompatibility. Osa-nijisseiki, a self-compatible mutant of Nijisseiki, produced S2-RNase, but did not produce S4-RNase. The absence of S4-RNase was also observed in self-compatible offsprings derived from Osa-Nijisseiki. These results suggest that Japanese pear in the family Rosaceae possesses a gametophytic self-incompatibility system involving an S-RNase, and that a reduction or lack of expression of S4-RNase in the style is responsible for the self-compatibility of Osa-Nijisseiki.
Abstract. At present, no suitable GIST model exists for the analysis of drug resistance or metastasis using established human gastrointestinal stromal tumor (GIST) cell lines or xenografts even though the molecular mechanisms of drug resistance, progression and metastasis require clarification. The aim of this study was to establish and characterize human GIST cell lines and xenografts that can be used for evaluating drug resistance or various new molecularly targeted therapies. GIST tissues from patients were cultured and implanted under the skin of NOG (NOD/Shi-scid, IL-2Rrnu) mice. Two new cell lines (GK1C and GK3C) and three xenografts (GK1X, GK2X and GK3X) were generated from these clinical samples. The established GIST cell lines and xenografts were investigated for tumorigenesis and imatinib sensitivity. These cell lines and xenografts showed characteristic GIST morphology and exhibited KIT expression profiles similar to those of the patient samples. In addition, these GIST cell lines and xenografts were sensitive to imatinib. In conclusion, new human GIST cell lines and xenografts were established and maintained through repeated passages. These models will enable further study of combination therapies and the mechanisms of resistance, and allow testing of novel targeted monotherapies and combination therapies. IntroductionHuman gastrointestinal stromal tumors (GISTs), mesenchymal tumors of the gastrointestinal tract (1), originate from the neoplastic transformation of interstitial cells of Cajal (ICC), which frequently express mutations in the c-KIT gene and occasionally in PDGFRA (2). The resulting mutations of KIT and PDGFRA receptors result in constitutive activation of receptor kinase activity leading to downstream effectors that deregulate cell proliferation and survival, thereby accelerating malignant progression (3). Surgery is currently the first-line treatment for patients with primary resectable GISTs (4,5). However, many patients develop recurrent or metastatic disease despite complete surgical resection (6) and since conventional chemotherapy or radiotherapy is usually ineffective (7). Thus, there are no ideal methods for treating such GISTs.Imatinib mesylate (imatinib) is a tyrosine kinase (TK) inhibitor that targets BCR-ABL, PDGFR, KIT, DDR and CSFR, and has been used to treat certain patients with KIT-positive GISTs having constitutive activating mutations in KIT (8). Although more than 80% of inoperable KIT-positive GIST patients exhibit clinical benefits from imatinib, the tumors in most of these patients will eventually progress (9,10). The activity of imatinib differs across various types of c-KIT and PDGFRA mutations, and secondary resistance in imatinibtreated patients often results from an emerging secondary mutation or amplification of c-KIT or PDGFRA (11-13). Approximately 50% of GISTs with secondary resistance to imatinib is caused by mutations in c- . Several studies have reported that the RTK switch is associated with imatinib-resistance, but the other mechanisms of secondary r...
Elastic neutron scattering experiments were carried out to investigate the magnetic structure and the critical behaviour of the mixed triangular antiferromagnetic system CsMn(Br 0.19 I 0.81 ) 3 , for which our previous magnetic measurement revealed the macroscopic anisotropy to be negligible. It is found that in the ordered state below T N = 8.29 K, the spin planes in which the spins lie with the 120 • structure are tilted from the basal plane, and that the average of the tilting angle φ is evaluated as cos 2 φ = 0.362, i.e. φ = 53 • . This result suggests that the present system is almost at the Heisenberg limit for the interaction. The critical exponent for the sublattice magnetization is obtained as β = 0.28 ± 0.02, which is in agreement with the value predicted for the chiral Heisenberg universality class.
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