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Splitting distance. As human cells begin to divide, their chromosomes align in the center, attached to poles at each end of the cell by structures called spindles, which are made up of small fibers called microtubules. The spindles maintain constant length by simultaneously building up one end while disassembling the other. New research from Tarun Kapoor’s Laboratory of Chemistry and Cell Biology has now identified how three proteins regulate the length of these spindles by playing a role in the disassembly of microtubule fibers. Using confocal fluorescence microscopy and fluorescent speckle microscopy, the researchers observed in real time that the microtubules, and therefore the spindles, lengthen when the proteins — dynein, dynactin and NuMA — are inhibited. The finding suggests that the three proteins regulate spindle length by helping a fourth protein, called Kif2a, target the appropriate end of the spindle.

Journal of Cell Biology, August 16, 2004

Improved therapy for amyloidosis. People with primary systemic amyloidosis, a disease of the bone marrow, develop deposits of protein fibers called amyloid, similar to those in the brains of Alzheimer’s patients, throughout their organs and tissues. Unlike Alzheimer’s, the disease kills quickly — median survival time is only 13 months. Now a team of researchers led by Madhav Dhodapkar has shown that treatment with drugs already used for multiple myeloma can more than double the survival time of amyloidosis patients. Between 1996 and 2003, the researchers treated 87 patients with high dose dexamethasone, and then maintained them on a regimen of dexamethasone and another myeloma drug, alpha-interferon. The patients survived for an average of 31 months. The study paves the way for dexamethasone becoming a standard therapy for amyloidosis. Dhodapkar is head of the Laboratory of Tumor Immunology and Immunotherapy.

Blood, August 12, 2004 online publication

How TB hides. Tuberculosis remains a threat long after the initial infection because the bacterium, M. tuberculosis, that causes it has evolved effective ways of dodging the immune system’s attacks. Research in both animals and humans has implicated a chemical messenger called gamma-interferon as a key weapon in immune system cells. Now, using a genetic screening technique known as differential signature-tagged transposon mutagenesis, which involves creating mutant TB strains and testing their virulence in immune-deficient mice, researchers in John McKinney’s Laboratory of Infection Biology have identified three M. tuberculosis genes used to repel the attacks driven by gamma-interferon. The researchers suggest that understanding TB’s immune evasion strategies could result in drugs that boost the immune system’s effectiveness against TB.

Infection and Immunity, September 2004

July 16, 2004

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