A gene, termed gli, was identified that is amplified more than 50-fold in a malignant glioma. The gene is expressed at high levels in the original tumor and its derived cell line and is located at chromosome 12 position (q13 to q14.3). The gli gene is a member of a select group of cellular genes that are genetically altered in primary human tumors.

African forest and savanna elephants are distinct species separated by a hybrid zone. Because hybridization can affect the systematic and conservation status of populations, we examined gene flow between forest and savanna elephants at 21 African locations. We detected cytonuclear dissociation, indicative of different evolutionary histories for nuclear and mitochondrial genomes. Both paternally (n = 205 males) and biparentally (n = 2,123 X-chromosome segments) inherited gene sequences indicated that there was deep genetic separation between forest and savanna elephants. Yet in some savanna locales distant from present-day forest habitats, many individuals with savanna-specific nuclear genotypes carried maternally transmitted forest elephant mitochondrial DNA. This extreme cytonuclear dissociation implies that there were ancient episodes of hybridization between forest females and savanna males, which are larger and reproductively dominant to forest or hybrid males. Recurrent backcrossing of female hybrids to savanna bulls replaced the forest nuclear genome. The persistence of residual forest elephant mitochondria in savanna elephant herds renders evolutionary interpretations based on mitochondrial DNA alone misleading and preserves a genomic record of ancient habitat changes.

Canine parvovirus (CPV) and feline panleukopenia virus (FPV) are important pathogens of dogs and cats. CPV is a new virus of dogs that first appeared in 1978, having arisen as a variant of a virus that infected cats or a related carnivore (31). CPV and FPV are over 99% identical in DNA sequence, but they differ in host range (29,30). Both viruses can infect feline and mink cells in tissue culture, but only CPV can efficiently infect cultured canine cells (30). FPV infection of dogs is restricted to certain cells of the bone marrow and thymus (30). The molecular determinants of CPV host range have been mapped to three regions on the surface of the capsid structure. Single amino acid changes in these regions lead to loss of the ability of CPV to infect canine, but not feline, cells (8,19). Mutation of residues Asn933Asp and Asn3233Asp in the VP2 capsid protein of FPV to the corresponding amino acids found in the VP2 protein of CPV allows that mutant to infect dog cells (8). The surface location of these host range determinants suggests that host range may be determined by the ability to bind a cell surface receptor or other cellular ligand (1).During natural infections, CPV and FPV infect actively dividing cells of the lymphopoietic system and the crypt cells of the intestine (reviewed in reference 22). Initial virus replication occurs in the oropharyngeal lymphoid tissue, and the virus then spreads hematogenously to other lymphoid organs and the intestine. Autonomous parvoviruses (including CPV and FPV) can replicate only in mitotically active cells during the S phase of the cell cycle (9), and so the target organs in vivo are those that contain actively dividing cell populations.

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