Patterns of plant species diversity during succession under different disturbance regimes

Summary I suggest that between-community variations in diversity patterns during succession in plant communities are due to the effects of selection on life history strategies under different disturbance regimes. Natural disturbances to plant communities are simultaneously a source of mortality for some individuals and a source of establishment sites for others. The plant community consists of a mosaic of disturbance patches (gaps) of different environmental conditions. The composition of the mosaic is described by the size-frequency distribution of the gaps and is dependent on the rates and scales of disturbance. The life-history strategies of plant species dependent on some form of disturbance for establishment of propagules should reflect this size-frequency distribution of disturbance patches. An extension of island biogeographic theory to encompass relative habitat area predicts that a community should be most rich in species adapted to growth and establishment in the spatially most common patch types. Changes in species diversity during succession following large scale disturbance reflect the prevalent life history patterns under historically common disturbance regimes. Communities in which the greatest patch area is in large-scale clearings (e.g. following fire) are most diverse in species establishing seedlings in xeric, high light conditions. Species diversity decreases during succession. Communities in which such large patches are rare are characterized by a large number of species that reach the canopy through small gaps and realtively few which regenerate in the large clearings. Diversity increases during succession following a large scale disturbance.Evidence from communities characterized by different disturbance regimes is summarized from the literature. This hypothesis provides an evolutionary mechanism with which to examine the changes in plant community structure during succession. Diversity peaks occurring at intermediate levels of disturbance as discussed by Connell and Huston are interpreted in this context.     

Phase response versus positive and negative division delay in animal cells

The time of median cell division in V79 Chinese hamster cells following high serum pulses was determined for two synchronous cell generations following mitotic selection. Differences in cell cycle time for each pair of pulse and control cultures were computed and plotted as a function of time of serum pulse. This phase response curve for hamster cells with an 8.5 h cell cycle shows a characteristic biphasic pattern. Beginning 0.5 h after mitotic selection, pulses with serum produce delays in the midpoint of the subsequent mitotic waves. Delay is maximum at 1.5 h. Delays give way abruptly to advances at 2.5 h and the amount of advance then decreases as pulses are given between 3 and 5 h into the cycle. At 5 h decreasing advances become delays, with increasing delays due to serum pulses occurring between 5 and 6 h. Delays again give way abruptly to advances at 6 h and again the amount of advance decreases through the late portion of the cycle. Pulses very late in the cycle appear to generate phase delays. This biphasic response to serum is interpreted as an expression of an underlying time-keeping oscillator whose period is nominally of 4 h duration.     

Etiology of two virus diseases of lilac (Syringa vulgaris L.) occurring in Czechoslovakia

Virus origin of lilac ringspot and chlorotic ringspot of lilac was identified serologically by means of double gel diffusion method. The former of these diseases is due to Arabis mosaic virus, the latter to a mixture of Arabis mosaic virus and cherry leaf roll virus. The occurrence of these viruses has been detected for the first time in Czechoslovakia.     

Lack of Liver X Receptors Leads to Cell Proliferation in a Model of Mouse Dorsal Prostate Epithelial Cell

Recent studies underline the implication of Liver X Receptors (LXRs) in several prostate diseases such as benign prostatic hyperplasia (BPH) and prostate cancer. In order to understand the molecular mechanisms involved, we derived epithelial cells from dorsal prostate (MPECs) of wild type (WT) or Lxrαβ−/− mice. In the WT MPECs, our results show that LXR activation reduces proliferation and correlates with the modification of the AKT-survival pathway. Moreover, LXRs regulate lipid homeostasis with the regulation of Abca1, Abcg1 and Idol, and, in a lesser extent, Srebp1, Fas and Acc. Conversely cells derived from Lxrαβ−/− mice show a higher basal phosphorylation and consequently activation of the survival/proliferation transduction pathways AKT and MAPK. Altogether, our data point out that the cell model we developed allows deciphering the molecular mechanisms inducing the cell cycle arrest. Besides, we show that activated LXRs regulate AKT and MAPK transduction pathways and demonstrate that LXRs could be good pharmacological targets in prostate disease such as cancer.     

Finite element analysis of active Eustachian tube function.

The inability to open the collapsible Eustachian tube (ET) has been related to the development of chronic otitis media. Although ET dysfunction may be due to anatomic and/or mechanical abnormalities, the precise mechanisms by which these structural properties alter ET opening phenomena have not been investigated. Previous investigations could only speculate on how these structural properties influence the tissue deformation processes responsible for ET opening. We have, therefore, developed a computational technique that can quantify these structure-function relationships. Cross-sectional histological images were obtained from eight normal adult human subjects, who had no history of middle ear disease. A midcartilaginous image from each subject was used to create two-dimensional finite element models of the soft tissue structures of the ET. ET opening phenomena were simulated by applying muscle forces on soft tissue surfaces in the appropriate direction and were quantified by calculating the resistance to flow (R(v)) in the opened lumen. A sensitivity analysis was conducted to determine the relative importance of muscle forces and soft-tissue elastic properties. Muscle contraction resulted in a medial-superior rotation of the medial lamina, stretching deformation in the Ostmann's fatty tissue, and lumen dilation. Variability in baseline R(v) values correlated with tissue size, whereas the functional relationship between R(v) and a given mechanical parameter was consistent in all subjects. ET opening was found to be highly sensitive to the applied muscle forces and relatively insensitive to cartilage elastic properties. These computational models have, therefore, identified how different tissue elements alter ET opening phenomena, which elements should be targeted for treatment, and the optimal mechanical properties of these tissue constructs.     

Hot spots and functional organization of human chromosomes

Summary Our working hypothesis is that the Q-darker human chromosome segments have higher gene densities than the bright regions. Especially prominent in this respect are six hot spots, the short Q-dark regions in 3p, 6p, 11q, 12q, 17q, and 19 (p or q), which have been chosen because their density of mitotic chiasmata is above 5. Chromosomes with gene-rich segments would act as trisomy lethals in very early embryos, whose spontaneous abortions would not be recognized. Containing active genes, the regions would be looped out in interphase and thus be more easily available for mitotic pairing and crossing-over.To test this hypothesis, correlations and partial correlations of the following parameters have been determined: the density of mitotic chiasmata, the number and density of localized genes, the incidence of trisomic abortions, the length of chromosomes, and their Q-brightness. Overall, the correlations and partial correlations agree with, but do not prove, the working hypothesis. Far stronger evidence for our hypothesis comes from the highly significant negative effect of hot spots on trisomic abortions which would act as a kind of trisomy lethal. The gene numbers on the hot-spot chromosomes as compared with the controls, on the other hand, are in the right direction, but the difference is not significant.This is paper No. 2161 from the Genetics Laboratory, University of Wisconsin. It was supported by National Institutes of Health (Washington) grants GM 22881, GM 15422-09, and, to Dr. Hans Ris, GM 04738; by grant IN-35P from the American Cancer Society, and by the U. W. Graduate Research Committee (Grant 101-4403). The photography was done by Mr. Walter Kugler, Jr.