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Vol 459|21 May

NATURE|Vol 2009May 2009


459|21 RESEARCH HIGHLIGHTS

dots. The authors say these observations reveal Carolina, and their colleagues focused on the was unknown. An elegant experiment now
that cadmium–selenide quantum dots are mouse visual cortex. They found that, unlike shows that they help pollinators to get a grip
paramagnetic — their magnetism is induced normal mice, when mice lacking Ube3A were on the plant surface.
and temporary — owing to interactions exposed to light, they lost synaptic plasticity Beverley Glover at the University of
between cadmium and the chemical groups — the learning-associated ability to change Cambridge, UK, and her colleagues observed
added to its surface to stifle its reactivity. The the strength of signals sent between brain cells the behaviour of bumblebees (Bombus
team saw no evidence to substantiate previous — in this area. But the Ube3A-deficient mice terrestris) on natural and artificial surfaces that
claims that quantum dots are ferromagnetic — recovered plasticity when deprived of visual were coated with flat or conical cells. When
that is, permanent magnets. stimuli, suggesting that Ube3A may help to the surfaces were presented at awkward angles,
maintain experience-dependent plasticity the bees grasped more easily and preferentially
EVOLUTION during periods of high brain activity. selected the textured surfaces. By making the
flower surface tractable for landing pollinators,
Home-field advantage

D. MANNING & B. GLOVER, UNIV. CAMBRIDGE


the authors suggest, conical epidermal cells
Am. Nat. 173, 579–588 (2009) increase the efficiency of pollination.
It has long been thought that for many
species, local populations are adapted to their CANCER BIOLOGY
local areas and would show greater fitness
there than anywhere else. However, some Cancer cop back on the beat
transplant studies have shown ‘out of town’ Cancer Cell 15, 376–388 (2009);
organisms doing better than the natives. Cancer Cell 15, 441–453 (2009)
Joe Hereford, now at the University Reactivating the cancer-fighting protein
of Maryland, College Park, looked at 74 p53 when it has been disabled in tumour cells
transplant studies containing 777 estimates can rein in cancer-promoting genes and kill
of local adaptation. He found that species cancer cells in culture.
showed local adaptation 71% of the time, and The protein is inactivated in many human
that, in general, native populations were 45% cancers, allowing tumour cells to escape
fitter than transplanted populations. And programmed cell death. Galina Selivanova of
species displaying high local adaptation were the Karolinska Institute in Stockholm and her
not always very unfit when transplanted. co-workers report that a compound called
RITA suppresses the expression of several
NEUROGENETICS cancer-causing genes by reactivating p53.
RITA also unleashes a host of cell-death-
Protecting plasticity promoting proteins, killing cancer cells.
Nature Neurosci. doi:10.1038/nn.2327 (2009) ECOLOGY Meanwhile, Klas Wiman, also of the
Angelman syndrome is a form of mental Stockholm Karolinska Institute, and his
retardation caused by mutations in the gene Pollinators get a grip colleagues show that another p53-reactivating
UBE3A. Scientists have discovered a role for Curr. Biol. doi:10.1016/j.cub.2009.04.051 (2009) compound, PRIMA-1, converted to reactive
the Ube3A protein that might explain the Animal-pollinated plants produce many compounds in living cells. One of the active
learning deficits associated with the disorder. cues and structures that help pollinators to metabolites reacts with the sulphur-containing
Benjamin Philpot of the University of navigate plant parts. Most flowering plants groups on the p53 protein, possibly restoring
North Carolina at Chapel Hill, Michael have cone-shaped cells on the surface of their mutated p53 to a normal conformation. p53 is
Ehlers at Duke University in Durham, North petals, but the specific function of these cells then able to trigger death in cancer cells.

JOURNAL CLUB to therapeutic applications, these


larger antibodies are hard to store
with the HIV gp120 antigen. To
select for neutralizing antibodies,
and CR6261 against influenza’s
haemagglutinin) in which only
William C. Hwang and deliver. But llama and other antibodies were raised against one heavy chains are involved in
Burnham Institute for Medical camelid antibodies demonstrate HIV subtype but cross-screened antigen binding — reminiscent of
Research, La Jolla, California superior heat-stability and against multiple subtypes. The the situation of llama antibodies.
A structural biologist has great solubility, without compromising researchers also included a These studies corroborate that
expectations for IIamas’ small affinity or specificity, making them competitive elution step to select the heavy chain alone can mediate
antibodies. an attractive alternative. antibodies that can compete broad neutralizing activity, and
Robin Weiss of University with binding by CD4, the primary invite speculation that this may
Llamas aren’t just unusual and College London and his colleagues HIV receptor on human T cells. be a special strategy engaged by
exotic looking: their antibodies are isolated three llama antibodies, It remains to be seen how these the human immune system to
also a reason for much excitement. known as ‘neutralizing’ antibodies, neutralizing antibodies fare in reach cryptic binding sites. Llama
Made entirely of heavy chains, that can broadly prevent multiple animal studies and where they antibodies may be even better
they are about half the size of HIV subtypes from infecting bind in atomic detail. suited for those hard-to-reach
those found in humans and many cells (A. Forsman et al. J. Virol. Intriguingly, there have targets.
other vertebrates, which are 82, 12069–12081; 2008). They been reports of several potent,
normally composed of both heavy began by creating an antibody broadly neutralizing human Discuss this paper at http://blogs.
and light chains. When it comes library from two llamas immunized antibodies (for example, F10 nature.com/nature/journalclub

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