Fluorescent differential display: Arbitrarily primed RT‐PCR fingerprinting on an automated DNA sequencer

Ito, Takashi; Kito, Keiji; Adati, Naoki; Mitsui, Yoshifuru; Hagiwara, Hiroaki; Sakaki, Yoshiyuki

doi:10.1016/0014-5793(94)00867-1

Cited by 182 publications

(117 citation statements)

References 15 publications

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“…Fluorescent differential display (FDD) was performed according to a previously described method (14). Anthers of S 8 and S 12 homozygotes of B. campestris were collected from flower buds of 1-10 mm in length that span most developmental stages.…”

Section: Methodsmentioning

confidence: 99%

The pollen determinant of self-incompatibility in Brassica campestris

Takayama

Shiba

Iwano

et al. 2000

Proc. Natl. Acad. Sci. U.S.A.

419

313

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Many flowering plants possess self-incompatibility (SI) systems that prevent inbreeding. In Brassica, SI is controlled by a single polymorphic locus, the S locus. Two highly polymorphic S locus genes, SLG (S locus glycoprotein) and SRK (S receptor kinase), have been identified, both of which are expressed predominantly in the stigmatic papillar cell. We have shown recently that SRK is the determinant of the S haplotype specificity of the stigma. SRK is thought to serve as a receptor for a pollen ligand, which presumably is encoded by another polymorphic gene at the S locus. We previously have identified an S locus gene, SP11 (S locus protein 11), of the S9 haplotype of Brassica campestris and proposed that it potentially encodes the pollen ligand. SP11 is a novel member of the PCP (pollen coat protein) family of proteins, some members of which have been shown to interact with SLG. In this work, we identified the SP11 gene from three additional S haplotypes and further characterized the gene. We found that (i) SP11 showed an S haplotype-specific sequence polymorphism; (ii) SP11 was located in the immediate flanking region of the SRK gene of the four S haplotypes examined; (iii) SP11 was expressed in the tapetum of the anther, a site consistent with sporophytic control of Brassica SI; and (iv) recombinant SP11 of the S9 haplotype applied to papillar cells of S9 stigmas, but not of S8 stigmas, elicited SI response, resulting in inhibition of hydration of cross-pollen. All these results taken together strongly suggest that SP11 is the pollen S determinant in SI.I n Brassica, SI is sporophytically controlled by a highly polymorphic locus, termed the S locus, with more than 100 haplotypes identified so far (1, 2). To date, two stigmatically expressed highly polymorphic genes have been identified at the S locus. One is the S locus glycoprotein (SLG) gene, which encodes a secreted glycoprotein abundantly present in the papillar cell of the stigma surface (3, 4), and the other is the S locus receptor kinase (SRK) gene, which encodes a putative receptor-like serine͞threonine protein kinase presumed to span the plasma membrane of the papillar cell (5). The predicted extracellular domain of SRK shares extensive sequence similarity with SLG. Results from our recent gain-of-function experiments have shown that SRK is the sole determinant of the S haplotype specificity of the stigma (6). SRK is thought to function as a receptor for the S determinant of pollen with the same S haplotype. Binding of SRK to the pollen S determinant then would elicit a signaling cascade in the papillar cell, leading to the rejection of self-pollen. Our recent study also has shown that the role of SLG is probably to enhance this recognition process, although how this is accomplished is not yet known (6).In contrast to the S determinant of the stigma, the pollen S determinant had long remained elusive. Doughty et al. (7,8) analyzed the pollen coat protein (PCP) of Brassica oleracea and identified a basic 7-kDa protein, termed PCP-A1 (protein 1 of cla...

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Section: Methodsmentioning

confidence: 99%

The pollen determinant of self-incompatibility in Brassica campestris

Takayama

Shiba

Iwano

et al. 2000

Proc. Natl. Acad. Sci. U.S.A.

419

313

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“…Di¡erential display of mRNAs by PCR [6,7] Reverse transcription (RT) was performed by incubation of 2. . The durations and temperatures used were 3 min at 94³C, 5 min at 40³C, and 1 min at 72³C for the initial cycle and 15 s at 94³C, 2 min at 40³C, and 1 min at 72³C for subsequent 25 cycles.…”

Section: Removal Of Contaminating Chromosomal Dnamentioning

confidence: 99%

Identification of a melanoma antigen, PRAME, as a BCR/ABL‐inducible gene

et al. 2000

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In order to elucidate molecular events in BCR/ABLinduced transformation, we adopted a polymerase chain reaction (PCR)-based technique of differential display and compared mRNA expression in human factor-dependent cells, TF-1, with that in factor-independent cells, ID-1, which were established from TF-1 cells by transfection of BCR/ABL. Cloning and sequencing of a gene which was upregulated in ID-1 cells revealed that the gene was identical to a melanoma antigen, PRAME. Our present study demonstrated that PRAME was markedly expressed in primary leukemic cells with chronic myeloid leukemia (CML) in blastic crisis and Philadelphia (Ph) + -acute lymphoblastic leukemia (ALL), in which BCR/ABL played an important role as a pathogenic gene. Moreover, comparison of PRAME expression among CD34 + cells with CML in blastic, accelerated, and chronic phases revealed a higher expression in CML in advanced phases. Thus PRAME was considered to be a good candidate for a marker of Ph + -leukemic blast cells as well as a new target antigen of leukemic blast cells that cytotoxic T cells can recognize.z 2000 Federation of European Biochemical Societies.

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“…In the present study, we adopted a rat experimental model for vasospasm 6 and used fluorescence differential display (FDD) 7 to identify differentially expressed genes and to evaluate the functional significance of such genes in vasospasm of the basilar artery. We identified that heat shock protein 72 (HSP72) was a gene highly sensitive to upregulation by cerebral vasospasm after SAH and that overexpression of HSP72 is a possible mechanism involved in the prevention and treatment of pathological conditions such as delayed cerebral vasospasm.…”

mentioning

confidence: 99%

Potential Role for Heat Shock Protein 72 in Antagonizing Cerebral Vasospasm After Rat Subarachnoid Hemorrhage

et al. 2004

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Background-Cerebral vasospasm can be defined as delayed-onset narrowing of the cerebral arteries that can occur after a spontaneous aneurysmal subarachnoid hemorrhage (SAH). Despite a large number of experimental and clinical investigations, the exact pathophysiology of vasospasm remains unknown. Using a fluorescence differential-display system, we have identified the gene encoding heat shock protein 72 (HSP72) as being highly upregulated by cerebral vasospasm. We therefore elucidated the role of the HSP72 gene in cerebral vasospasm in a rat experimental SAH model. Methods and Results-By angiography, cerebral vasospasm was detected from day 1, with maximal narrowing detected on day 2. Intracisternal injection of antisense HSP72 oligodeoxynucleotide led to specific inhibition of HSP72 gene expression and significantly aggravated cerebral vasospasm on days 2 and 3 of the angiographic studies. Oral administration of geranylgeranylacetone (GGA), an antiulcer drug, enhanced HSP72 induction and reduced cerebral vasospasm. Conclusions-These results suggest HSP72 plays a novel role in antagonizing delayed cerebral vasospasm after SAH and that GGA provides protective effects against delayed cerebral vasospasm, at least partly via induction of HSP72.

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Fluorescent differential display: Arbitrarily primed RT‐PCR fingerprinting on an automated DNA sequencer

Cited by 182 publications

References 15 publications

The pollen determinant of self-incompatibility in Brassica campestris

The pollen determinant of self-incompatibility in Brassica campestris

Identification of a melanoma antigen, PRAME, as a BCR/ABL‐inducible gene

Potential Role for Heat Shock Protein 72 in Antagonizing Cerebral Vasospasm After Rat Subarachnoid Hemorrhage

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