Biology subjects

Cros, A.

Publications and source records attributed to Cros, A..

3 recordsLinked to original sources

bioRxiv2026

Stony Coral Symbioses Show Variable Responses to Future Ocean Conditions

Coral reefs support over a quarter of marine species and nearly a billion people worldwide but are also among the ecosystems most threatened by anthropogenic impacts. There is long-standing debate about whether coral symbioses will be disrupted or respond adaptively under future ocean conditions. Using a factorial 2.5-year future-ocean mesocosm experiment across eight coral species representing the major coral lineages, we tracked symbiont community shifts within replicate fragments from the same individual coral. Some corals exhibited stochastic divergence consistent with dysbiosis, whereas others showed deterministic, thermally adaptive shifts. Heat stress generally reduced symbiont diversity and promoted predictable restructuring, supporting deterministic processes under moderate stress but stochastic dysbiosis under extreme conditions. We propose that adaptive and stochastic responses represent endpoints along a continuum of host-orchestrated symbiont sorting. This study bridges coral reef ecology with broader host-microbiome theory, offering an integrated perspective on how symbiotic systems may respond to environmental change. TeaserLong-term experiments reveal that corals follow distinct paths of symbiont change under heat stress, from adaptation to dysbiosis

molecular biology↗

bioRxiv2023

Homeostatic activation of Aryl Hydrocarbon Receptor by dietary ligands dampens cutaneous allergic responses by controlling Langerhans cells migration

Dietary compounds can affect the development of inflammatory responses at distant sites. However, mechanisms involved remain incompletely understood. Here we addressed the influence on allergic responses of dietary agonists of Aryl Hydrocarbon Receptor (AhR). In cutaneous papain-induced allergy, we found that lack of dietary AhR ligands exacerbates allergic responses. This phenomenon was tissue-specific, as airway allergy was unaffected by the diet. In addition, lack of dietary AhR ligands worsened asthma-like allergy in a model of atopic march. Mice deprived of dietary AhR ligands displayed impaired Langerhans cell migration, leading to exaggerated T cell responses. Mechanistically, dietary AhR ligands regulated the inflammatory profile of epidermal cells, without affecting barrier function. In particular, we evidenced TGF-{beta} hyperproduction in the skin of mice deprived of dietary AhR ligands, explaining Langerhans cell retention. Our work identifies an essential role for homeostatic activation of AhR by dietary ligands in the dampening of cutaneous allergic responses and uncovers the importance of the gutskin axis in the development of allergic diseases.

immunology↗

bioRxiv2021

Spatiotemporal manipulation of the mismatch repair system of Pseudomonas putida accelerates phenotype emergence

Developing complex phenotypes in industrially-relevant bacteria is a major goal of metabolic engineering, which encompasses the implementation of both rational and random approaches. In the latter case, several tools have been developed towards increasing mutation frequencies--yet the precise spatiotemporal control of mutagenesis processes continues to represent a significant technical challenge. Pseudomonas species are endowed with one of the most efficient DNA mismatch repair (MMR) systems found in bacteria. Here, we investigated if the endogenous MMR system could be manipulated as a general strategy to artificially alter mutation rates in Pseudomonas species. To bestow a conditional mutator phenotype in the platform bacterium Pseudomonas putida, we constructed inducible mutator devices to modulate the expression of the dominant-negative mutLE36K allele. Regulatable overexpression of mutLE36K in a broad-host-range, easy-to-cure plasmid format resulted in a transitory inhibition of the MMR machinery, leading to a significant increase (up to 438-fold) in mutation frequencies and a heritable fixation of genome mutations. Following such accelerated mutagenesis-followed-by selection approach, three phenotypes were successfully evolved: resistance to antibiotics streptomycin and rifampicin and reversion of a synthetic uracil auxotrophy. Thus, these mutator devices could be applied to accelerate evolution of metabolic pathways in long-term evolutionary experiments, alternating cycles of (inducible) mutagenesis coupled to selection schemes.

synthetic biology↗