Mechanism and Determinants of Amphipathic Helix-Containing Protein Targeting to Lipid Droplets

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Timed running speed of a cheetah (Acinonyx jubatus)

The speed of an adult cheetah was timed at 29ms^-1 (mean of three trials over a 201.2 m course, with a running start). This is the highest running speed that has been recorded reliably for any animal.     

Two Studies of Spirit Possession in Niger

Spirit Possession and Personhood among the Kel Ewey Tuareg. Susan J. Rasmussen. Cambridge: Cambridge University Press, 1995. 178 pp.
Embodying Colonial Memories: Spirit Possession, Power, and the Hauka in West Africa. Paul StoIIer. New York: Routledge, 1995. 226 pp.     

Small, Membrane-bound, Alternatively Spliced Forms of Ankyrin 1 Associated with the Sarcoplasmic Reticulum of Mammalian Skeletal Muscle

We have recently found that the erythroid ankyrin gene, Ank1, expresses isoforms in mouse skeletal muscle, several of which share COOH-terminal sequence with previously known Ank1 isoforms but have a novel, highly hydrophobic 72–amino acid segment at their NH₂ termini. Here, through the use of domainspecific peptide antibodies, we report the presence of the small ankyrins in rat and rabbit skeletal muscle and demonstrate their selective association with the sarcoplasmic reticulum. In frozen sections of rat skeletal muscle, antibodies to the spectrin-binding domain (anti-p65) react only with a 210-kD Ank1 and label the sarcolemma and nuclei, while antibodies to the COOH terminus of the small ankyrin (anti-p6) react with peptides of 20 to 26 kD on immunoblots and decorate the myoplasm in a reticular pattern. Mice homozygous for the normoblastosis mutation (gene symbol nb) are deficient in the 210-kD ankyrin but contain normal levels of the small ankyrins in the myoplasm. In nb/nb skeletal muscle, anti-p65 label is absent from the sarcolemma, whereas anti-p6 label shows the same distribution as in control skeletal muscle. In normal skeletal muscle of the rat, anti-p6 decorates Z lines, as defined by antidesmin distribution, and is also present at M lines where it surrounds the thick myosin filaments. Immunoblots of the proteins isolated with rabbit sarcoplasmic reticulum indicate that the small ankyrins are highly enriched in this fraction. When expressed in transfected HEK 293 cells, the small ankyrins are distributed in a reticular pattern resembling the ER if the NH₂-terminal hydrophobic domain is present, but they are uniformly distributed in the cytosol if this domain is absent. These results suggest that the small ankyrins are integral membrane proteins of the sarcoplasmic reticulum. We propose that, unlike the 210-kD form of Ank1, previously localized to the sarcolemma and believed to be a part of the supporting cytoskeleton, the small Ank1 isoforms may stabilize the sarcoplasmic reticulum by linking it to the contractile apparatus.     

Hybridization betweenPsidium guajava andP. guineense (Myrtaceae)

Psidium guajava andP. guineense are characterized, illustrated and contrasted. Population samples ofPsidium guajava andP. guineense and apparent hybrids were collected from four localities: two in Mexico, one in Honduras, and one in Argentina. Seven morphological characters, one micromorphological (stomatal density), and one chemical character (presence or absence of myricetin) that distinguish the parent species were found to be useful in the evaluation of specimens and population variation. Results were consistent with the hypothesis that hybridization occurs between these species, but in three localities it may not go beyond Fl ’s. Back crossing between hybrids andP. guajava was not detected at any locality.     

Autosomal dominant familial spastic paraplegia: tight linkage to chromosome 15q.

Autosomal dominant, uncomplicated familial spastic paraplegia (FSP) is a genetically heterogeneous disorder characterized by insidiously progressive lower-extremity spasticity. Recently, a locus on chromosome 14q was shown to be tightly linked with the disorder in one of three families. We performed linkage analysis in a kindred with autosomal dominant uncomplicated FSP. After excluding the chromosome 14q locus, we observed tight linkage of the disorder to a group of markers on chromosome 15q (maximum two-point lod score 9.70; theta = .05). Our results clearly establish the existence of a locus for autosomal dominant FSP in the centromeric region of chromosome 15q. Comparing clinical and genetic features in FSP families linked to chromosome 14q with those linked to chromosome 15q may provide insight into the pathophysiology of this disorder.