Dominique Pontier

NPR1 differentially interacts with members of the TGA/OBF family of transcription factors that bind an element of the PR-1 gene required for induction by salicylic acid.

NPR1 is a critical component of the salicylic acid (SA)-mediated signal transduction pathway leading to the induction of defense genes, such as the pathogenesis-related (PR)-1 gene, and enhanced disease resistance. Using a yeast two-hybrid screen, we identified several NPR1-interacting proteins (NIPs). Two of these NIPs are members of the TGA/OBF family of basic leucine zipper (bZIP) transcription factors; this family has been implicated in the activation of SA-responsive genes, including PR-1. Six TGA family members were tested and shown to differentially interact with NPR1: TGA2 and TGA3 showed strong affinity for NPR1; TGA5 and TGA6 exhibited weaker affinity; and TGA1 and TGA4 displayed little or no detectable interaction with NPR1, respectively. Interestingly, the amino-termini of these factors were found to decrease their stability in yeast and differentially affect their apparent affinity toward NPR1. The interacting regions on NPR1 and the TGA factors were also defined. Each of four point mutations in NPR1 that disrupt SA signaling in Arabidopsis completely blocked interaction of NPR1 with TGA2 and TGA3. TGA2 and TGA3 were also found to bind the SA-responsive element of the Arabidopsis PR-1 promoter. These results directly link NPR1 to SA-induced PR-1 expression through members of the TGA family of transcription factors.

Revealing cryptic spatial patterns in genetic variability by a new multivariate method

Increasing attention is being devoted to taking landscape information into account in genetic studies. Among landscape variables, space is often considered as one of the most important. To reveal spatial patterns, a statistical method should be spatially explicit, that is, it should directly take spatial information into account as a component of the adjusted model or of the optimized criterion. In this paper we propose a new spatially explicit multivariate method, spatial principal component analysis (sPCA), to investigate the spatial pattern of genetic variability using allelic frequency data of individuals or populations. This analysis does not require data to meet Hardy–Weinberg expectations or linkage equilibrium to exist between loci. The sPCA yields scores summarizing both the genetic variability and the spatial structure among individuals (or populations). Global structures (patches, clines and intermediates) are disentangled from local ones (strong genetic differences between neighbors) and from random noise. Two statistical tests are proposed to detect the existence of both types of patterns. As an illustration, the results of principal component analysis (PCA) and sPCA are compared using simulated datasets and real georeferenced microsatellite data of Scandinavian brown bear individuals (Ursus arctos). sPCA performed better than PCA to reveal spatial genetic patterns. The proposed methodology is implemented in the adegenet package of the free software R.

An analysis of demographic tactics in birds and mammals

Using field data on fecundity, age at first reproduction and adult life expectancy, we reconsider the so-called r-K gradient by analyzing relationships between these three demographic parameters in 80 mammal species and 114 bird species. After the allometric effect of adult body weight is removed, the three variables remain correlated. The existence of demographic tactics which are independent of adult body weight is demonstrated by multivariate analyses of these variables. These analyses confirm the importance of ecological and phylogenetic constraints. The main structure is a time-scale gradient ranking species according to turn-over, both in birds and mammals. A second gradient ranking species according to iteroparity level appears significantly both in birds and mammals. In mammals, this pattern is related to patterns of parental investment.

Frequency-dependent maintenance of left handedness in humans.

The percentage (10-13%) of left handedness in humans has apparently not changed since the Neolithic. Left handedness is heritable and appears to be repeatedly associated with some reduced fitness components; the persistence of left handedness implies that left handers have a fitness advantage in some situations. We propose that left handers have a frequency-dependent advantage in fights and for that reason a fitness advantage. To test this hypothesis, left handedness frequencies in the general population and in sporting individuals (both students and the sporting elite) have been compared, as sporting performance is likely to be a good indicator of fighting abilities. The higher proportion of left-handed individuals in interactive sports (reflecting some fighting elements), reaching 50% in some sports categories, but not in noninteractive sports, is consistent with the fighting hypothesis. The greater frequency of left handedness in males than in females is also consistent with this hypothesis, as male-male fights are universally more frequent than other combinations. The frequency-dependent advantage in fights of left handers might explain the stability of left handedness.

Genetic markers in the playground of multivariate analysis

Multivariate analyses such as principal component analysis were among the first statistical methods employed to extract information from genetic markers. From their early applications to current innovations, these approaches have proven to be efficient for the analysis of the genetic variability in various contexts such as human genetics, conservation and adaptation studies. However, because multivariate analysis is a wide and diversified area of statistics, choosing a method appropriate to both the data and to the question being asked can be difficult. Moreover, some particularities of genetic markers need to be taken into account when using multivariate methods. As a consequence, multivariate analyses are often used as black boxes, which results in frequent mistakes in the literature. In this review, we provide a critical analysis of the application of multivariate methods to genetic markers, using a general framework that unifies all these methods for the sake of clarity. First, we focus on some common mistakes in these applications and ways to avoid these pitfalls. We then detail the most critical particularities of allele frequencies that demand adaptations of multivariate methods, and we propose solutions to the subsequent problems. Finally, we tackle several questions of interest in which multivariate analysis has a great role to play, such as the study of the typological coherence of different genetic markers, or the investigation of spatial genetic patterns.

Argonaute quenching and global changes in Dicer homeostasis caused by a pathogen-encoded GW repeat protein

In plants and invertebrates, viral-derived siRNAs processed by the RNaseIII Dicer guide Argonaute (AGO) proteins as part of antiviral RNA-induced silencing complexes (RISC). As a counterdefense, viruses produce suppressor proteins (VSRs) that inhibit the host silencing machinery, but their mechanisms of action and cellular targets remain largely unknown. Here, we show that the Turnip crinckle virus (TCV) capsid, the P38 protein, acts as a homodimer, or multiples thereof, to mimic host-encoded glycine/tryptophane (GW)-containing proteins normally required for RISC assembly/function in diverse organisms. The P38 GW residues bind directly and specifically to Arabidopsis AGO1, which, in addition to its role in endogenous microRNA-mediated silencing, is identified as a major effector of TCV-derived siRNAs. Point mutations in the P38 GW residues are sufficient to abolish TCV virulence, which is restored in Arabidopsis ago1 hypomorphic mutants, uncovering both physical and genetic interactions between the two proteins. We further show how AGO1 quenching by P38 profoundly impacts the cellular availability of the four Arabidopsis Dicers, uncovering an AGO1-dependent, homeostatic network that functionally connects these factors together. The likely widespread occurrence and expected consequences of GW protein mimicry on host silencing pathways are discussed in the context of innate and adaptive immunity in plants and metazoans.

Is there geographical variation in human handedness

Right‐ and left‐handed individuals are present in all cultures. However, while it is known that handedness is a heritable trait, little is known about how handedness varies between populations—and without this knowledge, the significance of the left/right polymorphism is hard to interpret. We reviewed the literature to assess the extent of geographical variation of throwing or hammering handedness. These two tasks were chosen because they are present in all known cultures (unlike, for example, writing), and make sense within the context of several adaptive theories on the origin of laterality, or maintenance of handedness polymorphism, which state that tool or weapon manipulation are pivotal. A total of 81 samples were found with primary data on throwing or hammering handedness, spanning 14 countries and concerning more than 1,214,000 individuals studied between 1922 and 1998. A global logistic regression was performed to assess the significance of the country of the study, controlling for several potentially confounding variables (date of the study, sex and age of individuals). Country always had a significant effect, consistent with substantial geographical variation of throwing and hammering handedness. Curiously, left‐handedness frequency estimates for a given country were not always consistent across datasets, perhaps due to missing variables, such as educational level or socio‐economic status. Results are discussed in the context of the evolution of handedness and the significance of the current polymorphism.

Markers for hypersensitive response and senescence show distinct patterns of expression.

Controlled cellular suicide is an important process that can be observed in various organs during plant development. From the generation of proper sexual organs in monoecious plants to the hypersensitive response (HR) that occurs during incompatible pathogen interactions, programmed cell death (PCD) can be readily observed. Although several biochemical and morphological parameters have been described for various types of cell death in plants, the relationships existing between those different types of PCD events remain unclear. In this work, we set out to examine if two early molecular markers of HR cell death (HIN1 and HSR203J) as well as a senescence marker (SAG12) are coordinately induced during these processes. Our result indicates that although there is evidence of some cross-talk between both cell death pathways, spatial and temporal characteristics of activation for these markers during hypersensitive response and senescence are distinct. These observations indicate that these markers are relatively specific for different cell death programs. Interestingly, they also revealed that a senescence-like process seems to be triggered at the periphery of the HR necrotic lesion. This suggests that cells committed to die during the HR might release a signal able to induce senescence in the neighboring cells. This phenomenon could correspond to the establishment of a second barrier against pathogens. Lastly, we used those cell death markers to better characterize cell death induced by copper and we showed that this abiotic induced cell death presents similarities with HR cell death.

Activation of hsr203, a Plant Gene Expressed During Incompatible Plant-Pathogen Interactions, Is Correlated with Programmed Cell Death

hsr203J is a tobacco gene whose activation is rapid, highly localized, and specific for incompatible interactions between tobacco and the bacterial pathogen Ralstonia solanacearum. The effect of other hypersensitive response (HR)-inducing pathogens and elicitors has been tested with transgenic plants containing the hsr203J promoter-GUS reporter gene fusion, and confirms the generality of the preferential inducibility of the hsr203J gene promoter during incompatible interactions: bacterial and viral pathogens inducing an HR in tobacco were able to induce the promoter fusion, as were inducers of HR-like responses such as harpin, elicitins, and PopA1 proteins. A tomato hsr203 homologous cDNA was isolated (Lehsr203) and used to examine the effect of avr gene products on the expression of such genes. Lehsr203 was shown to be rapidly and transiently induced in leaves of the tomato Cf-9 line, following Avr9 product infiltration, but not in those of the Cf-0 line. Among potential effectors of HR or resistance such as H2O2, salicylic acid, methyl jasmonate, and 2,6-dichloro-isonicotinic acid (INA), none is able to induce a significant increase in promoter activation. In contrast, heavy metals that cause leaf necrosis can trigger such an activation. In addition, hsr203-GUS fusion expression is detected in transgenic tobacco lines expressing the bO gene and exhibiting spontaneous HR-like lesions. Taken together, these results demonstrate a strong correlation between hsr203 and genetically controlled cell death in tobacco and tomato. The expression of this gene should be a useful marker for programmed cell death occurring in response not only to diverse pathogens, but also to diverse death-triggering extracellular agents.

Generation Time: A Reliable Metric to Measure Life-History Variation among Mammalian Populations

Oli and Dobson proposed that the ratio between the magnitude and the onset of reproduction (F/α ratio) allows one to predict the relative importance of vital rates on population growth rate in mammalian populations and provides a reliable measure of the ranking of mammalian species on the slow‐fast continuum of life‐history tactics. We show that the choice of the ratio F/α is arbitrary and is not grounded in demographic theory. We estimate the position on the slow‐fast continuum using the first axis of a principal components analysis of all life‐history variables studied by Oli and Dobson and show that most individual vital rates perform as well as the F/α ratio. Finally, we find, in agreement with previous studies, that the age of first reproduction is a reliable predictor of the ranking of mammalian populations along the slow‐fast continuum and that both body mass and phylogeny markedly influence the generation time of mammalian species. We conclude that arbitrary ratios such as F/α correlate with life‐history types in mammals simply because life‐history variables are highly correlated in response to allometric, phylogenetic, and environmental influences. We suggest that generation time is a reliable metric to measure life‐history variation among mammalian populations and should be preferred to any arbitrary combination between vital rates.