SIGNALING EFFICACY DRIVES THE EVOLUTION OF LARGER SEXUAL ORNAMENTS BY SEXUAL SELECTION.

Why are there so few small secondary sexual characters? Theoretical models predict that sexual selection should lead to reduction as often as exaggeration, and yet we mainly associate secondary sexual ornaments with exaggerated features such as the peacock's tail. We review the literature on mate choice experiments for evidence of reduced sexual traits. This shows that reduced ornamentation is effectively impossible in certain types of ornamental traits (behavioral, pheromonal, or color-based traits, and morphological ornaments for which the natural selection optimum is no trait), but that there are many examples of morphological traits that would permit reduction. Yet small sexual traits are very rarely seen. We analyze a simple mathematical model of Fisher's runaway process (the null model for sexual selection). Our analysis shows that the imbalance cannot be wholly explained by larger ornaments being less costly than smaller ornaments, nor by preferences for larger ornaments being less costly than preferences for smaller ornaments. Instead, we suggest that asymmetry in signaling efficacy limits runaway to trait exaggeration

THE HANDICAP PROCESS FAVOURS EXAGGERATED, RATHER THAN REDUCED, SEXUAL ORNAMENTS.

Why are traits that function as secondary sexual ornaments generally exaggerated in size compared to the naturally selected optimum, and not reduced? Since they deviate from the naturally selected optimum, traits that are reduced in size will handicap their bearer, and could thus provide an honest signal of quality to a potential mate. Thus if secondary sexual ornaments evolve via the handicap process, current theory suggests that reduced ornamentation should be as frequent as exaggerated ornamentation, but this is not the case. To try to explain this discrepancy, we analyse a simple model of the handicap process. Our analysis shows that asymmetries in costs of preference or ornament with regard to exaggeration and reduction cannot fully explain the imbalance. Rather, the bias towards exaggeration can be best explained if either the signalling efficacy or the condition dependence of a trait increases with size. Under these circumstances, evolution always leads to more extreme exaggeration than reduction: though the two should occur just as frequently, exaggerated secondary sexual ornaments are likely to be further removed from the naturally selected optimum than reduced ornaments. This article is protected by copyright. All rights reserved

Gene mobility promotes the spread of resistance in bacterial populations

Theory predicts that horizontal gene transfer (HGT) expands the selective conditions under which genes spread in bacterial populations. Whereas vertically inherited genes can only spread by positively selected clonal expansion, mobile genetic elements can drive fixation of genes by infectious HGT. We tested this using populations of Pseudomonas fluorescens and the conjugative mercury resistance (Hg R) plasmid pQBR57. HGT expanded the selective conditions allowing the spread of Hg R: Chromosomal Hg R only increased in frequency under positive selection, whereas plasmid-encoded Hg R reached fixation with or without positive selection. Tracking plasmid dynamics over time revealed that the mode of Hg R inheritance varied across mercury environments. Under mercury selection, the spread of Hg R was driven primarily by clonal expansion while in the absence of mercury Hg R dynamics were dominated by infectious transfer. Thus, HGT is most likely to drive the spread of resistance genes in environments where resistance is useless

Neutrophils in cancer: neutral no more

Neutrophils are indispensable antagonists of microbial infection and facilitators of wound healing. In the cancer setting, a newfound appreciation for neutrophils has come into view. The traditionally held belief that neutrophils are inert bystanders is being challenged by the recent literature. Emerging evidence indicates that tumours manipulate neutrophils, sometimes early in their differentiation process, to create diverse phenotypic and functional polarization states able to alter tumour behaviour. In this Review, we discuss the involvement of neutrophils in cancer initiation and progression, and their potential as clinical biomarkers and therapeutic targets

Macrophages mediate the anti-tumor effects of the oncolytic virus HSV1716 in mammary tumors

Oncolytic viruses (OV) have been shown to activate the anti-tumor functions of specific immune cells like T cells. Here, we show OV can also reprogram TAMs to a less immunosuppressive phenotype. Syngeneic, immunocompetent mouse models of primary breast cancer were established using PyMT-TS1, 4T1 and E0771 cell lines and a metastatic model of breast cancer was established using the 4T1 cell line. Tumor growth and overall survival was assessed following intravenous administration of the OV, HSV1716 (a modified herpes simplex virus). Infiltration and function of various immune effector cells was assessed by NanoString, flow cytometry of dispersed tumors and immunofluorescence analysis of tumor sections. HSV1716 administration led to marked tumor shrinkage in primary mammary tumors and a decrease in metastases. This was associated with a significant increase in the recruitment/activation of cytotoxic T cells, a reduction in the presence of regulatory T cells and the reprograming of TAMs towards a pro-inflammatory, less immunosuppressive phenotype. These findings were supported by in vitro data demonstrating that human monocyte-derived macrophages (MDMs) host HSV1716 replication, and that this led to immunogenic macrophage lysis. These events were dependent on macrophage expression of proliferating cell nuclear antigen (PCNA). Finally, the anti-tumor effect of OV was markedly diminished when TAMs were depleted using clodronate liposomes. Together, our results show that TAMs play an essential role in support of the tumoricidal effect of the OV, HSV1716 - they both host viral replication via a novel, PCNA-dependent mechanism and are reprogramed to express a less immunosuppressive phenotype

The evolution of continuous variation in ejaculate expenditure strategy.

Sperm competition theory has largely focused on the evolution of ejaculate expenditure strategies across different species or populations or across discrete mating roles on which sperm competition operates differentially. Few studies have considered the extent to which male ejaculate expenditure is influenced by continuous change in male phenotype within a population. Here we model how optimal ejaculate expenditure responds to two sources of continuous variation: (1) the quantity of resources allocated by a male to mating within a breeding season and (2) the resource cost of obtaining a mate. We find that variation in the amount of resources available for mating does not alone produce selection for differing ejaculate investment strategies. However, when there is variation in the cost of obtaining a mate, males with a lower cost will be selected to invest fewer sperm per mating than males whose cost is higher. Any parameter decreasing this cost will also select for decreased ejaculate investment per mating. These results provide a novel insight into the evolution of male ejaculate expenditure strategies, revealing that individual constraints on the ability to secure matings can lead to variation in ejaculate expenditure even when the risk of sperm competition is the same for all males