An Intranuclear Microsporidium Associated with Acute Anemia in the Chinook Salmon,Oncorhynchus tshawytscha1

An intranuclear microsporidium is described from hemoblastic cells of the chinook salmon, Oncorhynchus tshawytscha. The infection is associated with an acute anemia in the fish. Up to 47% of the hemoblast nuclei were infected in anemic fish. The organisms, found only in spleen and kidney tissues, were 1–2 μm in diameter and consisted of vegetative and early sporulation forms. This microsporidium differs from known species which parasitize fish in its tissue location; however, the absence of mature spores and other life cycle stages precludes determination of its precise taxonomic identity.     

Water Relations of Seed Development and Germination in Muskmelon (Cucumis melo L.): VI. INFLUENCE OF PRIMING ON GERMINATION RESPONSES TO TEMPERATURE AND WATER POTENTIAL DURING SEED DEVELOPMENT

Seed priming (imbibition in water or osmotic solutions followedby redrying) generally accelerates germination rates upon subsequentre-imbibition, but the response to priming treatments can varyboth within and among seed lots. Seed maturity could influenceresponsiveness to priming, perhaps explaining variable primingeffects among developmentally heterogeneous seed lots. In thecurrent study, muskmelon (Cucumis melo L.) seeds at two stagesof development, maturing (40 d after anthesis (DAA)) and fullymature (60 DAA), were primed in 0?3 M KNO₃ for 48 h at 30 ?C,dried, and imbibed in polyethylene glycol 8000 solutions of0 to –1?2 MPa at 15, 20, 25, and 30 ?C. Germination sensitivitiesto temperature and water potential () were quantified as indicatorsof the influence of seed maturity and priming on seed vigour.Germination percentages of 40 and 60 DAA control seeds weresimilar in water at 30 ?C, but the mean germination rate (inverseof time to germination) of 40 DAA seeds was 50% less than thatof 60 DAA seeds. Germination percentages and rates of both 40and 60 DAA seeds decreased at temperatures below 25 ?C. Reductionsin also delayed and inhibited germination, with the 40 DAAseeds being more sensitive to low than the 60 DAA seeds. Primingsignificantly improved the performance of 40 DAA seeds at lowtemperatures and reduced , but had less effect on 60 DAA seeds.Priming lowered both the minimum temperature (T_b) and the minimum (_b) at which germination occurred. Overall, priming of 40 DAAseeds improved their germination performance under stress conditionsto equal or exceed that of control 60 DAA seeds, while 60 DAAseeds exhibited only modest improvements due to priming. Asthe osmotic environment inside mature fruits approximates thatof a priming solution, muskmelon seeds may be ‘primed’in situ during the late stage of development after maximum dryweight accumulation. Key words: Cucumis melo L., seed priming, germination, vigour, development, temperature     

A novel disorder caused by defective biosynthesis of N-linked oligosaccharides due to glucosidase I deficiency

Glucosidase I is an important enzyme in N-linked glycoprotein processing, removing specifically distal alpha-1,2-linked glucose from the Glc3Man9GlcNAc2 precursor after its en bloc transfer from dolichyl diphosphate to a nascent polypeptide chain in the endoplasmic reticulum. We have identified a glucosidase I defect in a neonate with severe generalized hypotonia and dysmorphic features. The clinical course was progressive and was characterized by the occurrence of hepatomegaly, hypoventilation, feeding problems, seizures, and fatal outcome at age 74 d. The accumulation of the tetrasaccharide Glc(alpha1-2)Glc(alpha1-3)Glc(alpha1-3)Man in the patient's urine indicated a glycosylation disorder. Enzymological studies on liver tissue and cultured skin fibroblasts revealed a severe glucosidase I deficiency. The residual activity was <3% of that of controls. Glucosidase I activities in cultured skin fibroblasts from both parents were found to be 50% of those of controls. Tissues from the patient subjected to SDS-PAGE followed by immunoblotting revealed strongly decreased amounts of glucosidase I protein in the homogenate of the liver, and a less-severe decrease in cultured skin fibroblasts. Molecular studies showed that the patient was a compound heterozygote for two missense mutations in the glucosidase I gene: (1) one allele harbored a G-->C transition at nucleotide (nt) 1587, resulting in the substitution of Arg at position 486 by Thr (R486T), and (2) on the other allele a T-->C transition at nt 2085 resulted in the substitution of Phe at position 652 by Leu (F652L). The mother was heterozygous for the G-->C transition, whereas the father was heterozygous for the T-->C transition. These base changes were not seen in 100 control DNA samples. A causal relationship between the alpha-glucosidase I deficiency and the disease is postulated.