The \u3cem\u3eChlamydomonas\u3c/em\u3e Genome Reveals the Evolution of Key Animal and Plant Functions

Chlamydomonas reinhardtii is a unicellular green alga whose lineage diverged from land plants over 1 billion years ago. It is a model system for studying chloroplast-based photosynthesis, as well as the structure, assembly, and function of eukaryotic flagella (cilia), which were inherited from the common ancestor of plants and animals, but lost in land plants. We sequenced the ∼120-megabase nuclear genome of Chlamydomonas and performed comparative phylogenomic analyses, identifying genes encoding uncharacterized proteins that are likely associated with the function and biogenesis of chloroplasts or eukaryotic flagella. Analyses of the Chlamydomonas genome advance our understanding of the ancestral eukaryotic cell, reveal previously unknown genes associated with photosynthetic and flagellar functions, and establish links between ciliopathy and the composition and function of flagella

The Marine Microbial Eukaryote Transcriptome Sequencing Project (MMETSP): illuminating the functional diversity of eukaryotic life in the oceans through transcriptome sequencing

International audienceCurrent sampling of genomic sequence data from eukaryotes is relatively poor, biased, and inadequate to address important questions about their biology, evolution, and ecology; this Community Page describes a resource of 700 transcriptomes from marine microbial eukaryotes to help understand their role in the world's oceans

Evidence for p53-like-mediated stress responses in green algae

Abstract The tumor suppressor protein, p53, plays a major role in cellular responses to stress and DNA damage in animals; despite its critical function, p53 homologs have not been identified in any algal or plant lineage. This study employs a functional and evolutionary approach to test for a p53 functional equivalent in green algae. Specifically, the study: (i) investigated the effect of two synthetic compounds known to interfere with p53 activity; (ii) searched for sequences with similarity to known p53-induced genes; and (iii) analyzed the expression pattern of one such sequence. The findings reported here suggest that a p53 functional equivalent is present and mediates cellular responses to stress in green algae

Sex as a response to oxidative stress: stress genes co-opted for sex

Despite a great deal of interest, the evolutionary origins and roles of sex remain unclear. Recently, we showed that in the multicellular green alga, Volvox carteri, sex is a response to increased levels of reactive oxygen species (ROS), which could be indicative of the ancestral role of sex as an adaptive response to stress-induced ROS. To provide additional support for the suggestion that sex evolved as a response to oxidative stress, this study addresses the hypothesis that genes involved in sexual induction are evolutionarily related to genes associated with various stress responses. In particular, this study investigates the evolutionary history of genes specific to the sexual induction process in V. carteri—including those encoding the sexual inducer (SI) and several SI-induced extracellular matrix (ECM) proteins. Surprisingly, (i) a highly diversified multigene family with similarity to the V. carteri SI and SI-induced pherophorin family is present in its unicellular relative, Chlamydomonas reinhardtii (which lacks both a SI and an ECM) and (ii) at least half of the 12 identified gene members are induced (as inferred from reported expressed sequence tags) under various stress conditions. These findings suggest an evolutionary connection between sex and stress at the gene level, via duplication and/or co-option

Sex as a response to oxidative stress: the effect of antioxidants on sexual induction in a facultatively sexual lineage.

The evolution of sex is one of the long-standing unsolved problems in biology. Although in many lineages sex is an obligatory part of the life cycle and is associated with reproduction, in prokaryotes and many lower eukaryotes, sex is facultative, occurs in response to stress and often involves the formation of a stress-resistant dormant form. The proximate and ultimate causes of the connection between stress and sex in facultatively sexual lineages are unclear. Because most forms of stress result in the overproduction of cellular reactive oxygen species (ROS), we address the hypothesis that this connection involves ROS and possibly reflects the ancestral role of sex as an adaptive response to the damaging effects of stress-induced ROS (i.e. oxidative stress). Here, we report that two antioxidants inhibit sexual induction in a facultatively sexual species - the multicellular green alga, Volvox carteri. Furthermore, the nature of the sex response and the effect of an iron chelator on sexual induction are consistent with sex being a response to the DNA-damaging effects of ROS. In addition, we present preliminary data to suggest that sex, cell-cycle arrest and apoptosis are alternative responses to increased levels of oxidative stress

In Vitro Model-Systems to Understand the Biology and Clinical Significance of Circulating Tumor Cell Clusters

The isolation of clusters of circulating tumor cells (CTCs) from cancer patients has recently challenged the accepted view that the initiation of secondary tumors during metastasis involves the dissemination of individual cancer cells. As such clusters appear to be more aggressive than single tumor cells, CTC clusters are now considered a main player in the metastatic process, and many studies are exploring their diagnostic, prognostic, and clinical significance. However, several technical challenges limit advances in this area. Here, we suggest the use of established cancer cell lines that grow as cell clusters in suspension as a complementary approach that can help in understanding the biology of CTC clusters and their clinical significance. We argue that the many similarities between these “surrogate” clusters and the CTC clusters isolated from patients (e.g., in terms of size, morphology, heterogeneous expression of epithelial and mesenchymal markers, and type of cell–cell junctions) make these cell lines ideal systems for the development of strategies aimed at preventing or slowing down the metastatic process by targeting CTC clusters

Synergistic inter-clonal cooperation involving crosstalk, co-option and co-dependency can enhance the invasiveness of genetically distant cancer clones

Abstract Background Despite intensive research, cancer remains a major health problem. The difficulties in treating cancer reflect the complex nature of this disease, including high levels of heterogeneity within tumours. Intra-tumour heterogeneity creates the conditions for inter-clonal competition and selection, which could result in selective sweeps and a reduction in levels of heterogeneity. However, in addition to competing, cancer clones can also cooperate with each other, and the positive effects of these interactions on the fitness of clones could actually contribute to maintaining the heterogeneity of tumours. Consequently, understanding the evolutionary mechanisms and pathways involved in such activities is of great significance for cancer treatment. This is particularly relevant for metastasis (i.e., tumor cell migration, invasion, dispersal and dissemination), which is the most lethal phase during cancer progression. To explore if and how genetically distant clones can cooperate during migration and invasion, this study used three distinct cancer cell lines with different metastatic potentials. Results We found that (i) the conditioned media from two invasive lines (breast and lung) increased the migration and invasion potential of a poorly metastatic line (breast), and (ii) this inter-clonal cooperative interaction involved the TGF-β1 signalling pathway. Furthermore, when the less aggressive line was co-cultured with the highly metastatic breast line, the invasive potential of both lines was enhanced, and this outcome was dependent on the co-option (through TGF-β1 autocrine-paracrine signalling) of the weakly metastatic clone into expressing an enhanced malignant phenotype that benefited both clones (i.e., a “help me help you” strategy). Conclusions Based on our findings, we propose a model in which crosstalk, co-option, and co-dependency can facilitate the evolution of synergistic cooperative interactions between genetically distant clones. Specifically, we suggest that synergistic cooperative interactions can easily emerge, regardless of the degree of overall genetic/genealogical relatedness, via crosstalk involving metastatic clones able to constitutively secrete molecules that induce and maintain their own malignant state (producer-responder clones) and clones that have the ability to respond to those signals (responder clones) and express a synergistic metastatic behaviour. Taking into account the lack of therapies that directly affect the metastatic process, interfering with such cooperative interactions during the early steps in the metastatic cascade could provide additional strategies to increase patient survival

Environmentally induced responses co-opted for reproductive altruism

Reproductive altruism is an extreme form of altruism best typified by sterile castes in social insects and somatic cells in multicellular organisms. Although reproductive altruism is central to the evolution of multicellularity and eusociality, the mechanistic basis for the evolution of this behaviour is yet to be deciphered. Here, we report that the gene responsible for the permanent suppression of reproduction in the somatic cells of the multicellular green alga, Volvox carteri, evolved from a gene that in its unicellular relative, Chlamydomonas reinhardtii, is part of the general acclimation response to various environmental stress factors, which includes the temporary suppression of reproduction. Furthermore, we propose a model for the evolution of soma, in which by simulating the acclimation signal (i.e. a change in cellular redox status) in a developmental rather than environmental context, responses beneficial to a unicellular individual can be co-opted into an altruistic behaviour at the group level. The co-option of environmentally induced responses for reproductive altruism can contribute to the stability of this behaviour, as the loss of such responses would be costly for the individual. This hypothesis also predicts that temporally varying environments, which will select for more efficient acclimation responses, are likely to be more conducive to the evolution of reproductive altruism