Population regulation in snowshoe hare and Canadian lynx: Asymmetric food web configurations between hare and lynx

The snowshoe hare and the Canadian lynx in the boreal forests of North America show 9- to 11-year density cycles. These are generally assumed to be linked to each other because lynx are specialist predators on hares. Based on time series data for hare and lynx, we show that the dominant dimensional structure of the hare series appears to be three whereas that of the lynx is two. The three-dimensional structure of the hare time series is hypothesized to be due to a three-trophic level model in which the hare may be seen as simultaneously regulated from below and above. The plant species in the hare diet appear compensatory to one another, and the predator species may, likewise, be seen as an internally compensatory guild. The lynx time series are, in contrast, consistent with a model of donor control in which their populations are regulated from below by prey availability. Thus our analysis suggests that the classic view of a symmetric hare–lynx interaction is too simplistic. Specifically, we argue that the classic food chain structure is inappropriate: the hare is influenced by many predators other than the lynx, and the lynx is primarily influenced by the snowshoe hare.

Lack of cell cycle regulation of telomerase activity in human cells

Conflicting reports have appeared concerning the cell cycle regulation of telomerase activity and its possible repression during quiescence and cell differentiation. We have reexamined these issues in an attempt to uncover the basis for the discrepancies. Variations in extracted telomerase activity during the cell cycle are not observed in cells sorted on the basis of DNA content. Variations are observed in cells synchronized using some biochemical cell cycle inhibitors, but only with those agents where cellular toxicity is evident. A progressive decline in telomerase activity is observed in cells whose growth rate is reduced from seven to eight population doublings per week to one to two doublings per week. Telomerase is largely absent in cells that truly exit the cell cycle and do not divide over the 7-day period. Although it is not necessary for all cell types to regulate telomerase in the same way, we conclude that in the immortal cultured cell lines examined, extracted telomerase activity does not change significantly during progression through the stages of the cell cycle. Telomerase activity generally correlates with growth rate and is repressed in cells that exit the cell cycle and become quiescent.

Regulation of dorsal fate in the neuraxis by Wnt-1 and Wnt-3a

Members of the Wnt family of signaling molecules are expressed differentially along the dorsal–ventral axis of the developing neural tube. Thus we asked whether Wnt factors are involved in patterning of the nervous system along this axis. We show that Wnt-1 and Wnt-3a, both of which are expressed in the dorsal portion of the neural tube, could synergize with the neural inducers noggin and chordin in Xenopus animal explants to generate the most dorsal neural structure, the neural crest, as determined by the expression of Krox-20, AP-2, and slug. Overexpression of Wnt-1 or Wnt-3a in the neuroectoderm of whole embryos led to a dramatic increase of slug and Krox-20-expressing cells, but the hindbrain expression of Krox-20 remained unaffected. Enlargement in the neural crest population could occur even when cell proliferation was inhibited. Wnt-5A and Wnt-8, neither of which is expressed in the dorsal neuroectoderm, failed to induce neural crest markers. Overexpression of glycogen synthase kinase 3, known to antagonize Wnt signaling, blocked the neural-crest-inducing activity of Wnt-3a in animal explants and inhibited neural crest formation in whole embryos. We suggest that Wnt-1 and Wnt-3a have a role in patterning the neural tube along its dorsoventral axis and function in the differentiation of the neural crest.

Widespread expression and estrogen regulation of PPEIA-3′ nuclear RNA in the rat brain

We previously identified a novel nuclear RNA species derived from the preproenkephalin (PPE) gene. This transcript, which we have named PPEIA-3′ RNA, hybridizes with probes directed at a region of PPE intron A downstream of an alternative germ-cell transcription start site, but does not contain PPE protein coding sequences. We now report that estrogen treatment of ovariectomized rats increases the expression of conventional PPE heteronuclear RNA, and also induces the expression of PPEIA-3′ RNA, apparently in separate cell populations within the ventromedial nucleus of the hypothalamus. Further, we show that cells expressing PPEIA-3′ are found in several neuronal groups in the rat forebrain and brainstem, with a distinct topographical distribution. High densities of PPEIA-3′ containing cells are found in the reticular thalamic nucleus, the basal forebrain, the vestibular complex, the deep cerebellar nuclei, and the trapezoid body, a pattern that parallels the distribution of atypical nuclear RNAs described by other groups. These results suggest that this diverse neuronal population shares a common set of nuclear factors responsible for the expression and retention of this atypical RNA transcript. The implication of these results for cell-specific gene transcription and regulation in the brain and the possible relationship of PPEIA-3′ RNA and other atypical nuclear RNAs is discussed.

Colony-forming progenitors from mouse olfactory epithelium: evidence for feedback regulation of neuron production.

The mammalian olfactory epithelium (OE) supports continual neurogenesis throughout life, suggesting that a neuronal stem cell exists in this system. In tissue culture, however, the capacity of the OE for neurogenesis ceases after a few days. In an attempt to identify conditions that support the survival of neuronal stem cells, a population of neuronal progenitors was isolated from embryonic mouse OE and cultured in defined serum-free medium. The vast majority of cells rapidly gave rise to neurons, which died shortly thereafter. However, when purified progenitors were co-cultured with cells derived from the stroma underlying the OE, a small subpopulation (0.07-0.1%) gave rise to proliferative colonies. A morphologically identifiable subset of these colonies generated new neurons as late as 7 days in vitro. Interestingly, development of these neuronal colonies was specifically inhibited when purified progenitors were plated onto stromal feeder cells in the presence of a large excess of differentiated OE neurons. These results indicate that a rare cell type, with the potential to undergo prolonged neurogenesis, can be isolated from mammalian OE and that stroma-derived factors are important in supporting neurogenesis by this cell. The data further suggest that differentiated neurons provide a signal that feeds back to inhibit production of new neurons by their own progenitors.

FAS is highly expressed in the germinal center but is not required for regulation of the B-cell response to antigen.

In establishing the memory B-cell population and maintaining self-tolerance during an immune response, apoptosis mediates the removal of early, low-affinity antibody-forming cells, unselected germinal center (GC) cells, and, potentially, self-reactive B cells. To address the role of the apoptosis-signaling cell surface molecule FAS in the B-cell response to antigen, we have examined the T-cell-dependent B-cell response to the carrier-conjugated hapten (4-hydroxy-3-nitrophenyl)acetyl (NP) in lpr mice in which the fas gene is mutated. High levels of FAS were expressed on normal GC B cells but the absence of FAS did not perturb the progressive decline in numbers of either GC B cells or extrafollicular antibody-forming cells. Furthermore, the rate of formation and eventual size of the NP-specific memory B-cell population in lpr mice were normal. The accumulation of cells with affinity-enhancing mutations and the appearance of high-affinity anti-NP IgG1 antibody in the serum were also normal in lpr mice. Thus, although high levels of FAS are expressed on GC B cells, FAS is not required for GC selection or for regulation of the major antigen-specific B-cell compartments. The results suggest that the size and composition of B-cell compartments in the humoral immune response are regulated by mechanisms that do not require FAS.