NatureArticle TheLorenzAttractorExists
NatureArticle TheLorenzAttractorExists
NatureArticle TheLorenzAttractorExists
a number of pumps, which may be the key The abundance of regulatory genes and
THOMAS MONINGER, UNIV. IOWA
to the bacterium’s ability to withstand anti- questions about the regulation of antibiotic
biotics in its human host. It has been pumps in P. aeruginosa call for investigators
suggested that Gram-negative bacteria, a to look into gene expression in this bac-
group to which P. aeruginosa belongs, can terium. To this end, the US Cystic Fibrosis
resist the lethal effects of many antibiotics Foundation is again taking a unique
by pumping them out of their cells faster approach, by building on its initial invest-
than the chemicals can accumulate. Mem- ment in P. aeruginosa genomics and under-
bers of the RND protein family of ‘multi- writing the cost of constructing a P. aerugi-
drug efflux’ pumps can render bacteria nosa gene-expression array. The charity
impervious to antibiotics4. It is not clear plans to make the array available to inter-
how or why these pumps evolved; perhaps ested researchers at a cost consistent with
they were first needed to eliminate nat- the budgets of academic scientists. It has
urally occurring environmental toxins. We also created a Cystic Fibrosis Bioinformatics
already knew of four RND pumps in P. Center, to support scientists using the arrays.
aeruginosa (E. coli has the same number, One hopes that the genomic information
whereas Mycobacterium tuberculosis, the reported by Stover et al.1, and the informa-
persistent pathogen that causes tuberculo- tion to come from the gene-expression
sis, has none). The sequencing project has analysis, will allow us finally to tame this
now revealed six more. testy pathogen. ■
When and where are these pumps active? E. Peter Greenberg is in the Department of
Figure 1 The rod-shaped Pseudomonas One idea is that they might be expressed Microbiology, College of Medicine, University of
aeruginosa on cultured epithelial cells from the when P. aeruginosa exists as a biofilm. These Iowa, Iowa City, Iowa 52242-1109, USA.
human respiratory tract. Each P. aeruginosa cell are stationary communities of bacteria that e-mail: [email protected]
measures about 0.5 by 2–3 mm. The bacterium are enclosed by a self-produced extracellular 1. Stover, C. K. et al. Nature 406, 959–964 (2000).
shows extraordinary nutritional versatility. matrix. When bacteria exist as biofilms, they 2. Fleischmann, R. D. et al. Science 269, 496–512 (1995).
3. The Pseudomonas Genome Project.
This might require the large number of genes can resist antimicrobial agents. A hypothesis
http://www.pseudomonas.com/
in its genome (the sequence of which is now to explain the persistence of P. aeruginosa in 4. Nikaido, H. Clin. Infect. Dis. 27, S32–S41 (1998).
published1) that are predicted to be involved in the lungs of a cystic fibrosis patient is that it 5. Costerton, W. C., Stewart, P. & Greenberg, E. P. Science 284,
regulating gene expression. may establish a biofilm in this environment5. 1318–1322 (1999).
M
alaria, an infectious disease responsi- that is found in the outer membrane of
the equations can always be split into a set of ble for an estimated 300 million to infected (but not uninfected) red blood cells,
contracting directions and a complementary 500 million clinical cases and 1.5 mil- and which helps to supply nutrients to the
set of expanding ones. But the Lorenz system lion to 2.7 million human deaths each year1, hungry parasite.
is not hyperbolic. Singular hyperbolicity is caused by a single-celled parasite that It has long been known that following
replaces the idea of expanding directions in invades the red blood cells of its host. In the the invasion of a human red blood cell by
the flow by the condition that part of the flow 48 hours after it invades a red blood cell, the Plasmodium falciparum — the most virulent
should expand in volume. If some sides of a parasite grows to many times its original size, of the four malaria parasites that are infec-
box expand and others contract, the volume and then divides to produce 20–30 new para- tious to humans — the membrane of the
may nonetheless expand if the amount of sites. To fuel this high rate of growth and infected cell undergoes a dramatic increase
expansion beats the amount of contraction. multiplication, the malaria parasite needs in its permeability to a range of small sol-
So singular hyperbolicity is less restrictive nutrients from outside the infected cell. utes, both charged and uncharged3–6. The
than hyperbolicity. However, a normal red blood cell is unable to pathways responsible for the increased
Tucker’s other important idea is using take up at least some nutrients fast enough to permeability have previously been shown
computer calculations in a rigorous way to satisfy the parasite’s voracious appetite. On to have a strong preference for negatively
establish certain features of the geometry of page 1001 of this issue2, Desai and colleagues charged ions (anions) over positively charged
the solutions of differential equations — provide new insights into how this problem ions (cations), and to be blocked by drugs
normal numerics plus precise error esti- is solved. They describe a versatile channel known to inhibit anion-selective channels6
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