Momilactones are bioactive diterpenoids that contribute to plant defense against pathogens and allelopathic interactions between plants. Both cultivated and wild grass species ofOryzaandEchinochloa crus-galli(barnyard grass) produce momilactones using a biosynthetic gene cluster (BGC) in their genomes. The bryophyteCalohypnum plumiforme(formerlyHypnum plumaeforme) also produces momilactones, and the bifunctional diterpene cyclase geneCpDTC1/HpDTC1,which is responsible for the production of the diterpene framework, has been characterized. To understand the molecular architecture of the momilactone biosynthetic genes in the moss genome and their evolutionary relationships with other momilactone-producing plants, we sequenced and annotated theC. plumiformegenome. The data revealed a 150-kb genomic region that contains two cytochrome P450 genes, theCpDTC1/HpDTC1gene and the “dehydrogenase momilactone A synthase” gene tandemly arranged and inductively transcribed following stress exposure. The predicted enzymatic functions in yeast and recombinant assay and the successful pathway reconstitution inNicotiana benthamianasuggest that it is a functional BGC responsible for momilactone production. Furthermore, in a survey of genomic sequences of a broad range of plant species, we found that momilactone BGC is limited to the two grasses (OryzaandEchinochloa) andC. plumiforme, with no synteny among these genomes. These results indicate that while the gene cluster inC. plumiformeis functionally similar to that in rice and barnyard grass, it is likely a product of convergent evolution. To the best of our knowledge, this report of a BGC for a specialized plant defense metabolite in bryophytes is unique.
Five types of lymphoid neoplasms in calves are described. Four cases with clinicopathologic features of the "calf form of lymphoma" were diagnosed as precursor B or T lymphoblastic leukemia. These neoplasms were positive for terminal deoxynucleotidyl transferase (TdT), a marker for immature lymphocytes. The fifth case (thymic B cell lymphoma) was also TdT positive, but was characterized by massive neoplastic involvement of the thymus. The sixth case involved bovine leukemia virus (BLV). As in the majority of previously reported BLV-associated cases, the neoplastic cells expressed CD5, and atypical giant cells were detected. Instead of enzootic bovine leukosis, in which at least two immunophenotypically distinct entities are included, a diagnosis of BLV-associated pleomorphic B-1 B cell lymphoma was made. The last case, involving an epitheliotropic γδ T cell lymphoma, was characterized by epitheliotropism in the gastrointestinal tract and WC1 expression. Since several histologic types of lymphoid neoplasm occur in calves, the term "calf form of lymphoma" should be abandoned for accurate diagnosis.
The majority of sinonasal non-Hodgkin's lymphomas (NHLs) are thought to originate from T-cell lineage. However, they often express natural killer (NK)-cell markers so that their origin still remains obscure. In this study, cell type of sinonasal NHLs were characterized by immunohistochemical and Southern blot analyses. We examined nine patients with sinonasal NHL. Six patients with tonsillar or pharyngeal non-B-cell lymphomas served as a control group. Immunohistochemical study showed that all nine cases of sinonasal NHL were CD56+CD2+, whereas controls were CD56-CD2+. According to the rearrangement of T- cell receptors (TCRs) and expression of CD3 markers, the sinonasal NHL cases were classified into three groups: TCR-CD56(Leu-19)+CD3(Leu4)- NHL (three patients), TCR-CD56+CD3+ NHL (five patients), and TCR+CD56+CD3+ NHL (one patient). In contrast, control patients' NHLs were TCR+CD56-CD3+. These results imply that eight cases of TCR-CD56+ sinonasal NHL are of NK-cell lineage. Among these eight cases, TCR- CD56+CD3+ cases (five of eight patients) were rather similar to the phenotype of fetal NK cells. From these results, the majority of sinonasal NHLs seem to originate from varying maturation stages of NK- cell lineage.
The majority of sinonasal non-Hodgkin's lymphomas (NHLs) are thought to originate from T-cell lineage. However, they often express natural killer (NK)-cell markers so that their origin still remains obscure. In this study, cell type of sinonasal NHLs were characterized by immunohistochemical and Southern blot analyses. We examined nine patients with sinonasal NHL. Six patients with tonsillar or pharyngeal non-B-cell lymphomas served as a control group. Immunohistochemical study showed that all nine cases of sinonasal NHL were CD56+CD2+, whereas controls were CD56-CD2+. According to the rearrangement of T- cell receptors (TCRs) and expression of CD3 markers, the sinonasal NHL cases were classified into three groups: TCR-CD56(Leu-19)+CD3(Leu4)- NHL (three patients), TCR-CD56+CD3+ NHL (five patients), and TCR+CD56+CD3+ NHL (one patient). In contrast, control patients' NHLs were TCR+CD56-CD3+. These results imply that eight cases of TCR-CD56+ sinonasal NHL are of NK-cell lineage. Among these eight cases, TCR- CD56+CD3+ cases (five of eight patients) were rather similar to the phenotype of fetal NK cells. From these results, the majority of sinonasal NHLs seem to originate from varying maturation stages of NK- cell lineage.
Anhidrotic ectodermal dysplasia (EDA) is a genetic disease characterized by the absence or hypoplasia of hair, teeth and eccrine sweat glands that has been reported in humans, the tabby mouse mutants, cattle and dogs. The EDA gene on the X chromosome encodes a protein, ectodysplasin-A (EDA), which is responsible for EDA. Here we describe a novel mutation of the EDA gene in which a 19 bp deletion in exon 1 in male Holstein calves demonstrated the phenotypic features of EDA. The dam and the grand-dam of the affected calves were heterozygous for this deletion. It is assumed that this deletion close to the start codon confuses all transcripts, and leads to the complete loss of pleiotropic functions of the bovine EDA gene. These results suggest that this mutation might be useful as animal models for the investigation of the pathogenic mechanisms of the anhidrotic ectodermal dysplasia.
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