Interrelació entre evolució i desenvolupament embrionari

El desenvolupament embrionari és un procés complex pel qual una cèl·lula ou es transforma, després de la fecundació, en un organisme adult. Aquestes transformacions estan controlades per xarxes d'interacció entre gens. L'evolució també es un procés complex en el que la forma canvia al llarg del temps en una població. Així, tant el desenvolupament com l'evolució són processos de canvi, un durant la vida d'un organisme i l'altre entre generacions. Aquests dos processos estan íntimament lligats perquè qualsevol canvi en l'evolució apareix primer com un canvi en el desenvolupament d'un individu en una població. La direcció de l'evolució està determinada, d'una banda, pel desenvolupament (que determina quins canvis morfològics són possibles) i, de l'altre, per la selecció natural (que determina quins d'aquests canvis passaran a les properes generacions). Així, l'estudi del desenvolupament és crucial per entendre com els gens determinen les característiques del cos i com funciona l'evolució.El desarrollo embrionario es un proceso complejo por el cual una célula huevo se transforma, tras la fecundación, en un organismo adulto. Estas transformaciones están controladas por redes de interacción entre genes. La evolución también es un proceso complejo en el que la forma cambia a lo largo del tiempo en una población. Así, tanto el desarrollo como la evolución son procesos de cambio, uno durante la vida de un organismo y el otro entre generaciones. Estos dos procesos están íntimamente ligados porque cualquier cambio en la evolución aparece primero como un cambio en el desarrollo de un individuo en una población. La dirección de la evolución está determinada, por un lado, por el desarrollo (que determina qué cambios morfológicos son posibles) y, por el otro, por la selección natural (que determina cuáles de estos cambios pasarán a las próximas generaciones). Así, el estudio del desarrollo es crucial para entender cómo los genes determinan las características del cuerpo y cómo funciona la evolución

Un nou model simula l'efecte dels gens en el desenvolupament dels organismes

Investigadors de la UAB i de la Universitat de Helsinki han desenvolupat un model matemàtic capaç de descriure, amb més precisió i realisme que mai, l'acció dels gens sobre l'organització de les cèl·lules i, per tant, sobre la morfologia de tot l'organisme. El model descriu com un grup de cèl·lules idèntiques s'organitzen per formar una estructura complexa tridimensional, com es produeixen les diferències entre individus a partir de petis canvis genètics, i quines són les interaccions entre gens responsables d'aquestes diferències. La recerca ha estat publicada a Nature.Investigadores de la UAB y de la Universidad de Helsinki han desarrollado un modelo matemático capaz de describir, con más precisión y realismo que nunca, la acción de los genes sobre la organización de las células y, por tanto, sobre la morfología de todo el organismo. El modelo describe cómo un grupo de células idénticas se organizan para formar una estructura compleja tridimensional, cómo se producen las diferencias entre individuos a partir de pequeños cambios genéticos, y cuáles son las interacciones entre genes responsables de estas diferencias. La investigación ha sido publicada en Nature.Researchers at UAB and University of Helsinki have developed a mathematical model able to describe how a group of identical cells organise themselves to form a complex three-dimensional structure, how differences between individuals occur based on small genetic changes, and which gene interactions are responsible for these differences

Mechanisms of Pattern Formation, Morphogenesis, and Evolution

This chapter introduces the diversity of ways in which developmental mechanisms lead to pattern formation and morphogenesis. Developmental mechanisms are described as gene networks in which at least one of the genes affects some cell behavior (cell division, cell adhesion, apoptosis, cell contraction, cell growth, signal and extracellular matrix secretion, etc.). These mechanisms mediate one of the most important processes in development: the transformation of specific distributions of cell types in space (starting with the zygote) into other, often more complex, spatial distributions of cell types (later developmental stages ending up in the adult). This chapter explains in detail why genes alone are unable to account for pattern formation and why they require cell behaviors and epigenetic factors. Three main types of developmental mechanisms are described in this respect: autonomous, inductive, and morphogenetic. This chapter also explains how these three types of mechanisms are combined in animal development and how these different combinations lead to different kinds of phenotypic variation and morphological evolution. It is concluded that understanding the mechanisms of development is crucial to have a more complete evolutionary theory in which extant phenotypes can be explained based not only on natural selection but also on what phenotypic variation can be produced by development in each generation.Peer reviewe

Why call it developmental bias when it is just development?

The concept of developmental constraints has been central to understand the role of development in morphological evolution. Developmental constraints are classically defined as biases imposed by development on the distribution of morphological variation. This opinion article argues that the concepts of developmental constraints and developmental biases do not accurately represent the role of development in evolution. The concept of developmental constraints was coined to oppose the view that natural selection is all-capable and to highlight the importance of development for understanding evolution. In the modern synthesis, natural selection was seen as the main factor determining the direction of morphological evolution. For that to be the case, morphological variation needs to be isotropic (i.e. equally possible in all directions). The proponents of the developmental constraint concept argued that development makes that some morphological variation is more likely than other (i.e. variation is not isotropic), and that, thus, development constraints evolution by precluding natural selection from being all-capable. This article adds to the idea that development is not compatible with the isotropic expectation by arguing that, in fact, it could not be otherwise: there is no actual reason to expect that development could lead to isotropic morphological variation. It is then argued that, since the isotropic expectation is untenable, the role of development in evolution should not be understood as a departure from such an expectation. The role of development in evolution should be described in an exclusively positive way, as the process determining which directions of morphological variation are possible, instead of negatively, as a process precluding the existence of morphological variation we have no actual reason to expect. This article discusses that this change of perspective is not a mere question of semantics: it leads to a different interpretation of the studies on developmental constraints and to a different research program in evolution and development. This program does not ask whether development constrains evolution. Instead it asks questions such as, for example, how different types of development lead to different types of morphological variation and, together with natural selection, determine the directions in which different lineages evolve.Non peer reviewe

Evolution of the G Matrix under Nonlinear Genotype-Phenotype Maps

Publisher Copyright: © 2022 The University of Chicago.The G matrix is a statistical summary of the genetic basis of a set of traits and a central pillar of quantitative genetics. A persistent controversy is whether G changes slowly or quickly over time. The evolution of G is important because it affects the ability to predict, or reconstruct, evolution by selection. Empirical studies have found mixed results on how fast G evolves. Theoretical work has largely been developed under the assumption that the relationship between genetic variation and phenotypic variation—the genotype-phenotype map (GPM)—is linear. Under this assumption, G is expected to remain constant over long periods of time. However, according to developmental biology, the GPM is typically complex and nonlinear. Here, we use a GPM model based on the development of a multicellular organ to study how G evolves. We find that G can change relatively fast and in qualitative different ways, which we describe in detail. Changes can be particularly large when the population crosses between regions of the GPM that have different properties. This can result in the additive genetic variance in the direction of selection fluctuating over time and even increasing despite the eroding effect of selection.Peer reviewe

How complexity increases in development : An analysis of the spatial-temporal dynamics of Gene expression in Ciona intestinalis

The increase in complexity in an embryo over developmental time is perhaps one of the most intuitive processes of animal development. It is also intuitive that the embryo becomes progressively compartmentalized over time and space. In spite of this intuitiveness, there are no systematic attempts to quantify how this occurs. Here, we present a quantitative analysis of the compartmentalization and spatial complexity of Ciona intestinalis over developmental time by analyzing thousands of gene expression spatial patterns from the ANISEED database. We measure compartmentalization in two ways: as the relative volume of expression of genes and as the disparity in gene expression between body parts. We also use a measure of the curvature of each gene expression pattern in 3D space. These measures show a similar increase over time, with the most dramatic change occurring from the 112-cell stage to the early tailbud stage. Combined, these measures point to a global pattern of increase in complexity in the Ciona embryo. Finally, we cluster the different regions of the embryo depending on their gene expression similarity, within and between stages. Results from this clustering analysis, which partially correspond to known fate maps, provide a global quantitative overview about differentiation and compartmentalization between body parts at each developmental stage. (C) 2017 Elsevier B.V. All rights reserved.Peer reviewe

The Evolution of Cleavage in Metazoans

Cleavage is the earliest developmental stage. During this stage, the fertilized oocyte gives rise to a cluster of smaller cells (blastomeres) with a particular spatial pattern (a cleavage pattern). Different metazoan species have different cleavage patterns, but most of them fit into a small set of basic types.Peer reviewe

Cell signaling stabilizes morphogenesis against noise

Embryonic development involves gene networks, extracellular signaling, cell behaviors (cell division, adhesion, etc.) and mechanical interactions. How should these be coordinated to lead to complex and robust morphologies? To explore this question, we randomly wired genes and cell behaviors into a huge number of networks in EmbryoMaker. EmbryoMaker is a computational model of animal development that simulates how the 3D positions of cells, i.e. morphology, change over time due to such networks. We found that any gene network can lead to complex morphologies if this activates cell behaviors over large regions of the embryo. Importantly, however, for such complex morphologies to be robust to noise, gene networks should include cell signaling that compartmentalizes the embryo into small regions where cell behaviors are regulated differently. If, instead, cell behaviors are equally regulated over large regions, complex but non-robust morphologies arise. We explain how compartmentalization enhances robustness and why it is a general feature of animal development. Our results are consistent with theories proposing that robustness evolved by the co-option of gene networks and extracellular cell signaling in early animal evolution.Peer reviewe

Adaptation and Conservation throughout the Drosophila melanogaster Life-Cycle

Previous studies of the evolution of genes expressed at different life-cycle stages of Drosophila melanogaster have not been able to disentangle adaptive from nonadaptive substitutions when using nonsynonymous sites. Here, we overcome this limitation by combining whole-genome polymorphism data from D. melanogaster and divergence data between D. melanogaster and Drosophila yakuba. For the set of genes expressed at different life-cycle stages of D. melanogaster, as reported in modENCODE, we estimate the ratio of substitutions relative to polymorphism between nonsynonymous and synonymous sites (alpha) and then alpha is discomposed into the ratio of adaptive (omega(a)) and nonadaptive (omega(na)) substitutions to synonymous substitutions. We find that the genes expressed in mid- and late-embryonic development are the most conserved, whereas those expressed in early development and postembryonic stages are the least conserved. Importantly, we found that low conservation in early development is due to high rates of nonadaptive substitutions (high omega(na)), whereas in postembryonic stages it is due, instead, to high rates of adaptive substitutions (high omega(a)). By using estimates of different genomic features (codon bias, average intron length, exon number, recombination rate, among others), we also find that genes expressed in mid- and late-embryonic development show the most complex architecture: they are larger, have more exons, more transcripts, and longer introns. In addition, these genes are broadly expressed among all stages. We suggest that all these genomic features are related to the conservation of mid- and late-embryonic development. Globally, our study supports the hourglass pattern of conservation and adaptation over the life-cycle.Peer reviewe

Patterned Anchorage to the Apical Extracellular Matrix Defines Tissue Shape in the Developing Appendages of Drosophila

How tissues acquire their characteristic shape is a fundamental unresolved question in biology. While genes have been characterized that control local mechanical forces to elongate epithelial tissues, genes controlling global forces in epithelia have yet to be identified. Here, we describe a genetic pathway that shapes appendages in Drosophila by defining the pattern of global tensile forces in the tissue. In the appendages, shape arises from tension generated by cell constriction and localized anchorage of the epithelium to the cuticle via the apical extracellular-matrix protein Dumpy (Dp). Altering Dp expression in the developing wing results in predictable changes in wing shape that can be simulated by a computational model that incorporates only tissue contraction and localized anchorage. Three other wing shape genes, narrow, tapered, and lanceolate, encode components of a pathway that modulates Dp distribution in the wing to refine the global force pattern and thus wing shape.Peer reviewe