Stability of forest biodiversity

Two hypotheses to explain potentially high forest biodiversity have different implications for the number and kinds of species that can coexist and the potential loss of biodiversity in the absence of speciation. The first hypothesis involves stabilizing mechanisms, which include tradeoffs between species in terms of their capacities to disperse to sites where competition is weak, to exploit abundant resources effectively and to compete for scarce resources. Stabilization results because competitors thrive at different times and places. An alternative, 'neutral model' suggests that stabilizing mechanisms may be superfluous. This explanation emphasizes 'equalizing' mechanisms, because competitive exclusion of similar species is slow. Lack of ecologically relevant differences means that abundances experience random 'neutral drift', with slow extinction. The relative importance of these two mechanisms is unknown, because assumptions and predictions involve broad temporal and spatial scales. Here we demonstrate that predictions of neutral drift are testable using palaeodata. The results demonstrate strong stabilizing forces. By contrast with the neutral prediction of increasing variance among sites over time, we show that variances in post-Glacial tree abundances among sites stabilize rapidly, and abundances remain coherent over broad geographical scales.     

Functional genetic analysis of mouse chromosome 11

Now that the mouse and human genome sequences are complete, biologists need systematic approaches to determine the function of each gene. A powerful way to discover gene function is to determine the consequence of mutations in living organisms. Large-scale production of mouse mutations with the point mutagen N-ethyl-N-nitrosourea (ENU) is a key strategy for analysing the human genome because mouse mutants will reveal functions unique to mammals, and many may model human diseases. To examine genes conserved between human and mouse, we performed a recessive ENU mutagenesis screen that uses a balancer chromosome, inversion chromosome 11 (refs 4, 5). Initially identified in the fruitfly, balancer chromosomes are valuable genetic tools that allow the easy isolation of mutations on selected chromosomes. Here we show the isolation of 230 new recessive mouse mutations, 88 of which are on chromosome 11. This genetic strategy efficiently generates and maps mutations on a single chromosome, even as mutations throughout the genome are discovered. The mutations reveal new defects in haematopoiesis, craniofacial and cardiovascular development, and fertility.     

Sequence of Plasmodium falciparum chromosomes 1, 3-9 and 13

Since the sequencing of the first two chromosomes of the malaria parasite, Plasmodium falciparum, there has been a concerted effort to sequence and assemble the entire genome of this organism. Here we report the sequence of chromosomes 1, 3-9 and 13 of P. falciparum clone 3D7--these chromosomes account for approximately 55% of the total genome. We describe the methods used to map, sequence and annotate these chromosomes. By comparing our assemblies with the optical map, we indicate the completeness of the resulting sequence. During annotation, we assign Gene Ontology terms to the predicted gene products, and observe clustering of some malaria-specific terms to specific chromosomes. We identify a highly conserved sequence element found in the intergenic region of internal var genes that is not associated with their telomeric counterparts.     

The landing of the NEAR-Shoemaker spacecraft on asteroid 433 Eros

The NEAR-Shoemaker spacecraft was designed to provide a comprehensive characterization of the S-type asteroid 433 Eros (refs 1,2,3), an irregularly shaped body with approximate dimensions of 34 x 13 x 13 km. Following the completion of its year-long investigation, the mission was terminated with a controlled descent to its surface, in order to provide extremely high resolution images. Here we report the results of the descent on 12 February 2001, during which 70 images were obtained. The landing area is marked by a paucity of small craters and an abundance of 'ejecta blocks'. The properties and distribution of ejecta blocks are discussed in a companion paper. The last sequence of images reveals a transition from the blocky surface to a smooth area, which we interpret as a 'pond'. Properties of the 'ponds' are discussed in a second companion paper. The closest image, from an altitude of 129 m, shows the interior of a 100-m-diameter crater at 1-cm resolution.     

Growth induced by pulsatile infusion of an amidated fragment of human growth hormone releasing factor in normal and GHRF-deficient rats

The discovery of human pancreatic growth hormone releasing factors (GHRFs) and subsequent characterization of human hypothalamic GHRF has led to studies on the role of these peptides in stimulating growth hormone (GH) release, and attempts to use GHRF peptides to increase growth rates in short children are already underway. However, there is no experimental evidence in animals that exogenous GHRF promotes growth in vivo. Although anaesthetized rats release GH reproducibly in response to GHRF injections, the responses in conscious male rats are much more variable, perhaps because of their highly episodic endogenous GH secretory pattern. In contrast, female rats secrete GH in a more continuous pattern and respond reproducibly to repeated injections of GHRF. We report here that it is possible to establish a 'male' type of GH secretory pattern in normal female rats by long-term pulsatile intravenous (i.v.) infusions of the active human GHRF fragment GHRF (1-29)NH2. We found that this treatment accelerates growth and increases pituitary GH content, whereas continuous infusions of this GHRF fragment at the same daily dose are ineffective. Pulsatile, but not continuous GHRF also stimulates growth in animals made GHRF-deficient by neonatal monosodium glutamate treatment. Thus exogenous GHRF will stimulate growth in both GHRF-deficient and normal animals provided it is administered in an appropriate pattern.