On Similarities between Biological and Social Evolutionary Mechanisms: Mathematical Modeling

In the first part of this article we survey general similarities and<br>differences between biological and social macroevolution. In the<br>second (and main) part, we consider a concrete mathematical<br>model capable of describing important features of both biological<br>and social macroevolution. In mathematical models of historical<br>macrodynamics, a hyperbolic pattern of world population growth<br>arises from non-linear, second-order positive feedback between<br>demographic growth and technological development. This is more<br>or less identical with the working of the collective learning<br>mechanism. Based on diverse paleontological data and an analogy<br>with macrosociological models, we suggest that the hyperbolic<br>character of biodiversity growth can be similarly accounted for by<br>non-linear, second-order positive feedback between diversity<br>growth and the complexity of community structure, suggesting<br>the presence within the biosphere of a certain analogue of the<br>collective learning mechanism. We discuss how such positive<br>feedback mechanisms can be modelled mathematically

Sun1, but not A-type lamins, participates in the positioning of cone photoreceptor nuclei.

<p>A) Immunolocalization of A- and B-type lamins, Sun1, Sun2 and Nesprin2 within the mature ONL of adult retinas (top) or the developing ONL of P8 retinas (bottom). Cartoons: summary of immunolocalization experiments (blue: positive, white: negative). Scale bars: 20 μm. B, C) Immunolocalization of cone nuclei within the ONL of P32 Sun1^−/− (B) and P21 LMNA^−/− (C) retinas in comparison to their respective wild-type littermates. See <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0047180#pone-0047180-g003" target="_blank">Figure 3F and S</a>4 for quantification of cone nuclei positioning in these genotypes. Scale bars: 20 μm.</p

LINC complexes mediate the positioning of cone photoreceptor nuclei.

<p>A) Genetic strategy used to derive Tg(<i>^HRGP</i>^floxCMV-EGFP-KASH2) mice expressing EGFP-KASH2 specifically in cone photoreceptors. B) CAR immunostaining of P26 Tg(CMV-LacZ/EGFP-KASH2) and Tg(<i>^HRGP</i>^floxCMV-EGFP-KASH2) littermates retinas. Lower panel: Zoomed view of the basal side of the ONL showing CAR⁺/EGFP-KASH2⁺ nuclei in the outer plexiform layer. Yellow arrows in merged image point to OS atop IS of cone nuclei expressing high levels of EGFP-KASH2. Scale bars: 50 μm and 20 μm (lower panel). C) Basalmost EGFP-KASH2⁺ cone nuclei express a significantly higher level of EGFP-KASH2 recombinant protein in comparison to their apical counterparts (p<0.001, Student's t-test). Error bars represent ±SEM from measurement of EGFP intensities of basal and apical nuclei from three random fields within ONL two Tg(<i>^HRGP</i>^floxCMV-EGFP-KASH2) littermate retinas. D) Mispositioned EGFP-KASH2⁺ nuclei are significantly less elongated. Maximal Feret diameters were significantly smaller in basal (n = 85) vs. apical (n = 68) EGFP-KASH2+ nuclei (p<0.01, Student's t-test). Error bars represent ±SEM from measurements of two random fields within two Tg(<i>^HRGP</i>^floxCMV-EGFP-KASH2) littermate retinas. E) Depiction and measurement of inclusion zones for the indicated genotypes (see text for details). Red nuclei are ectopic (centroids outside the inclusion zone) while green nuclei are correctly positioned (centroids within the inclusion zone). F) Percentages of ectopic (red) and of correctly positioned (green) nuclei of populations of n cone nuclei of the indicated genotypes. G) The size of cone populations estimated by the number of cone outer segments labeled with CAR in 4 month-old Tg(CMV-LacZ/EGFP-KASH2) and Tg(<i>^HRGP</i>^floxCMV-EGFP-KASH2) littermates retinas are not significantly different (p>0.05, Student's t-test). Error bars represent ±SEM from the counting of 5 random fields within littermate retinas of each genotype.</p

A model for the molecular mechanism underlying the baso-apical migration of cone precursor nuclei.

<p>A) Between P4 and P12, cone precursors nuclei initially move towards the basal side of the developing ONL, a movement potentially mediated by microtubules plus-end directed kinesins, before moving back to the apical side. Inset: Depiction of a B-type lamins/Sun1-2/Nesprin2 network of macromolecular complexes that transduce forces generated by dyneins to move cone nuclei precursors back towards the apical side of the developing ONL. B) Disruption of LINC complexes displaces endogenous Nesprin2 (inset) leading to the uncoupling of cone nuclei to dynein. As a result, cone nuclei fail to migrate apically and mislocalize on the inner edge of the ONL. Basalmost localization of these nuclei interferes with the architecture of cone pedicles.</p

Transgenic expression pattern of Tg(CMV-LacZ/EGFP-KASH2) retinas.

<p>A) Depiction of the organization of LINC complexes that physically couple the nuclear lamina to peripheral cytoskeletal networks and molecular motors. INM, ONM: Inner and outer nuclear membrane, respectively. PNS: perinuclear space. Nesprin α, β and γ depict shorter isoforms originating from the alternative splicing of Nesprin 1 and 2 genes. B) Top: depiction of the CMV-LacZ/EGFP-KASH2 genetic construct (see text for details). Left panel: Transgenic expression pattern detected by X-gal staining of Tg(CMV-LacZ/EGFP-KASH2) retinal flat mount. Note the preferential transgenic expression on the dorsal side of the retina. Right panel: X-gal staining of vertical slices. Note the restriction of transgenic expression to the outer nuclear layer. ONL: outer nuclear layer; INL: inner nuclear layer; GCL: ganglion cell layer. C) LacZ/V5 is mostly expressed in rods and a few cones. Vertical sections of P32 Tg(CMV-LacZ/EGFP-KASH2) were immunostained with anti-Cone arrestin (CAR) and anti-V5 antibodies. The arrow points to a CAR+/V5+ transgenic cone. Scale bars: 50 μm.</p

EGFP-KASH2⁺ cone precursor nuclei fail to migrate towards the apical surface of the developing ONL.

<p>A) Cone opsin staining of P8 Tg(CMV-LacZ/EGFP-KASH2) retinas. Note the scattering of wild-type cone nuclei within the apical two thirds of the developing ONL. B) Same experiment on P8 Tg(<i>^HRGP</i>^floxCMV-EGFP-KASH2) littermate retinas. Note the basalmost mislocalization of cone nuclei expressing high levels of EGFP-KASH2. Arrowheads point to pyramid-shaped pedicles. Inset (lower panels): pyramid-shaped pedicles are present beneath wild type or EGFP-KASH2⁺ nuclei that are still confined within the ONL (nucleus 3) but not beneath EGFP-KASH2⁺ cones whose nuclei occupy basalmost locations (nuclei 1 and 2). Scale bars: 20 μm (upper panel) and 10 μm (lower panel).</p

Basalmost localization of EGFP-KASH2+ cone nuclei alters cone terminals morphology in adult Tg(<i>^HRGP</i>^<b>flox</b>CMV-EGFP-KASH2) retina.

<p>A) Maximum intensity projection of a Z-stack series acquired from Tg(<i>^HRGP</i>^floxCMV-EGFP-KASH2) retina stained with either anti-CAR (A) or Alexa594-PNA (B). Arrows in A) denote the staining pattern of CAR underneath EGFP-KASH2⁺ cones nuclei located within the OPL. As shown in B), these nuclei also displayed weaker or no basal PNA signal. Sale bars: 10 μm. C) PNA signal underneath EGFP-KASH2⁺ cone nuclei located within the OPL (EGFP-KASH2⁺) is significantly weaker (p<0.01) by comparison to PNA signals measured from regions devoid of EGFP-KASH2⁺ nuclei (EGFP-KASH2⁻).</p

Additional file 1: of Chronic obstructive pulmonary disease, bronchial asthma and allergic rhinitis in the adult population within the commonwealth of independent states: rationale and design of the CORE study

“Study questionnaires used in the CORE study” contains description of the patient-reported questionnaires used in the CORE study. (DOCX 16 kb