Characterisation of a variant of zucchini yellow fleck virus (ZYFV), a potyvirus causing a wilt disease of melons in Israel*

A flexuous filamentous virus 750 nm in length was isolated from field-grown melons (Cucumis melo L.) and squirting cucumber (Ecballium elaterium L.). Infection of melon seedlings of most commercial varieties resulted in a lethal wilting, but late infections gave dieback. The virus infected systemically all economically important cucurbit crops. Its coat protein consists of a single polypeptide, 34 500 D in size, encapsidating a single stranded RNA genome of 10.1 kb. Antiserum against the Italian zucchini yellow fleck virus (ZYFV) reacted specifically with the Israeli isolate in both ISEM and Western blot. The virus was aphid transmissible in a non-persistent manner. Based on host range, host reaction and serological data, it is suggested that the virus described is an Israeli variant of ZYFV.     

Biochemical and Ultrastructural Changes in Tetrahymena pyriformis During Starvation*

SYNOPSIS. Certain of the ultrastructural and biochemical changes occurring during the first 25 hr of starvation in Tetrahymena pyriformis were studied. Ultrastructurally, numerous profiles of degenerating mitochondria were seen in the early stages of starvation. The presence of oxidizable substrate such as glucose and acetate did not prevent this degeneration. Numerous large nucleoli were formed, many of which seemed to be passing into the cytoplasm as forming autophagic vacuoles. There was a transient increase in Oil Red O-positive bodies, presumably lipid (triglycerides). The extent and duration of this increase were pronounced in the presence of acetate. The lipid droplets appeared to arise within the cisternae of the endoplasmic reticulum. Lipid reserves were apparently utilized prior to carbohydrates, as the disappearance of lipid droplets preceded glycogen utilization, both in the presence of acetate and in the absence of exogenous substrate. A considerable loss of cellular protein also occurred. In cells from inorganic medium supplemented with glucose, glycogen occupied much of the cell, leaving only islands of cell organelles. Acid phosphatase was localized, ultrastructurally, mainly in autophagic vacuoles which contained mitochondria and other cell organelles, and in association with small, double-membraned structures which seemed to be sequestering small areas of cytoplasm. Such sequestered areas also appeared within larger autophagic vacuoles. Residual bodies containing concentric whorls of myelin-like membranes surrounding a more solid core accumulated during starvation. Acid phosphatase activity decreased in amount but not in specific activity. The specific activity of cathespin doubled or tripled, but there was little change in total enzyme.     

Surface Alterations of Cells Carrying RNA Tumour Virus Genetic Information

CELLS transformed by the DNA tumour viruses, polyoma virus and SV40, are agglutinated by lectins such as wheat germ agglutinin¹, concanavalin A (Con A)² and soybean agglutinin³. Agglutination in these cases presumably reflects changes in the cell surface related to the transformed properties of the cell; studies with a temperature-dependent mutant of polyoma virus has shown that cell surface changes are controlled by viral genes⁴. Here we describe experiments in which we investigated the agglutinability of cells transformed by RNA tumour viruses. One recent report had suggested that cells transformed by RNA tumour viruses were not specifically agglutinated⁵, whereas a second more recent report claimed the specific agglutination of cells transformed by RSV⁶. We find that transformed rat, mouse and cat cells that replicate the sarcoma-leukaemia virus complex of murine (MSV) and feline (FeSV) origin are strongly agglutinated by Con A, but mouse and human cells that replicate the murine and feline leukaemia virus components alone are not agglutinated. The ability to agglutinate is rapidly acquired by normal mouse cells on infection with the murine sarcoma virus at a rate that parallels virus replication. In contrast to the results obtained with cells producing virus, non-virus-producing transformed hamster and mouse cells that synthesize virus-specific RNA are either not agglutinated or are agglutinated to a lesser degree. These results suggest that the cell surface alterations responsible for agglutination are not necessarily associated with the transformed state of the cell, but rather with the possession of sarcoma virus-specific information.     

Experimental Boron Neutron Capture Therapy for Melanoma: Systemic Delivery of Boron to Melanotic and Amelanotic Melanoma

The boron-containing melanin precursor analogue p-boronophenylalanine (BPA) has previously been shown to selectively deliver boron to pigmented murine melanomas when administered in a single intragastric dose. If boron neutron capture therapy is to become a clinically useful method of radiation therapy for human malignant melanoma, the boron carrier must be capable of delivering useful amounts of boron to remote tumor sites (metastases) and to poorly pigmented melanomas. We have now determined the ability of BPA to accumulate in several nonpigmented melanoma models including human melanoma xenografts in nude mice. The absolute amount of boron in the nonpigmented melanomas was about 50% of that observed in the pigmented counterparts but was still selectively concentrated in the tumor relative to normal tissues in amounts sufficient for effective neutron capture therapy. Single intragastric doses of BPA resulted in selective localization of boron in the amelanotic Greene melanoma carried in the anterior chamber of the rabbit eye and in a pigmented murine melanoma growing in the lungs. The ratio of the boron concentration in these tumors to the boron concentration in the immediately adjacent normal tissue was in the range of 3:1 to 4:1. These distribution studies support the proposal that boron neutron capture therapy may be useful as a regional therapy for malignant melanoma.     

Land clearing reduces gene flow in the granite outcrop‐dwelling lizard,Ctenophorus ornatus

An important question for the conservation of species dwelling in fragmented habitats is whether changes to the intervening landscape create a barrier to gene flow. Here, we make use of the spatial distribution of the granite outcrop‐dwelling lizard, Ctenophorus ornatus, to compare inferred levels of gene flow between outcrops in a nature reserve with that between outcrops in the adjacent agricultural land. Genetic variation, relatedness and subdivision were compared within groups of individuals from different outcrops similar in size and distance apart at each site. In the agricultural land, we found significantly lower genetic variation within outcrops and greater genetic differentiation between outcrops than in the reserve. Further, the rate at which genetic divergence between outcrops increased over geographical distance was significantly greater in the agricultural land than in the reserve. We also found that individuals were more closely related within outcrops but more distantly related between outcrops in the cleared land. These effects occur over a small spatial scale with an average distance between outcrops of less than five kilometres. Thus, even though land clearing around the outcrops leaves outcrop size unchanged, it restricts gene flow, reducing genetic variation and increasing population structure, with potentially negative consequences for the long‐term persistence of the lizards on these outcrops.