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Bautista, R.

Publications and source records attributed to Bautista, R..

3 recordsLinked to original sources

Tomato leaf transcriptomic changes promoted by long-term water scarcity stress can be largely prevented by a fungal-based biostimulant

Water availability is by far the leading environmental factor limiting crop productivity worldwide. The use of cell-free microbial culture filtrates (CF) as biostimulant is gaining ground as a safe and ecologically sound approach to improving crop yields while reducing anthropogenic pressure. However, their action mechanisms remain unknown. Here we found that foliar application of Trichoderma harzianum CF enhanced fruit yield, root growth and photosynthesis in plants of a commercial tomato cultivar grown under long-term water deficit in Mediterranean greenhouse conditions. To investigate the biochemical and molecular mechanisms underlying this phenomenon, we adopted an integrative and systems biology approach to characterize plants grown under optimal and suboptimal irrigation conditions (OIC and SOIC, respectively) with or without the fungal CF treatment. Water shortage promoted changes in the levels of drought stress-related signalling molecules, and in the transcriptome of leaves that potentially accounted for the physiochemical differences recorded between OIC- and SOIC-grown plants. Notably, many of these changes were largely prevented by the foliar application of fungal CF to SOIC-grown plants, including the expression of ca. 50% of the expression of water scarcity-responsive genes. These genes did not respond to CF in OIC-grown plants, indicating that the transcriptomic response to CF is strongly determined by the water status of the plant. Taken together, the data provided evidence that foliar application of fungal CF improves yield and long-term water scarcity tolerance by preventing a large portion of the stress-induced transcriptional response, rendering plants "blind", or less sensitive to water stress.

plant biology↗

Ghost admixture in eastern gorillas

Archaic admixture has had a significant impact on human evolution with multiple events across different clades, including from extinct hominins such as Neanderthals and Denisovans into modern humans. Within the great apes archaic admixture has been identified in chimpanzees and bonobos, but the possibility of such events has not been explored in other species. Here, we address this question using high-coverage whole genome sequences from all four extant gorilla subspecies, including six newly sequenced eastern gorillas from previously unsampled geographic regions. Using Approximate Bayesian Computation (ABC) with neural networks to model the demographic history of gorillas, we find a signature of admixture from an archaic ghost lineage into the common ancestor of eastern gorillas, but not western gorillas. We infer that up to 3% of the genome of these individuals is introgressed from an archaic lineage that diverged more than 3 million years ago from the common ancestor of all extant gorillas. This introgression event took place before the split of mountain and eastern lowland gorillas, likely more than 40 thousand years ago, and may have influenced perception of bitter taste in eastern gorillas. When comparing the introgression landscapes of gorillas, humans and bonobos, we find a consistent depletion of introgressed fragments on the X chromosome across these species. However, depletion in protein-coding content is not detectable in eastern gorillas, possibly as a consequence of stronger genetic drift in this species.

evolutionary biology↗

ATR-I774Yfs*5 promotes genomic instability through micronuclei formation

Although mismatch repair (MMR) defects are associated with high risk of malignancy, the specific oncogenic drivers pertinent to MMR-affected cancers are poorly characterized. The heterozygous ATR-I774Yfs*5 mutation, the result of strand slippage in a poly-A tract of the Ataxia Telangiectasia and Rad3 related (ATR) gene, is overexpressed in MMR-defective malignancies including colorectal carcinoma (CRC) and is the most common ATR mutation in cancer. Here, we explore the contribution of ATR-I774Yfs*5 to genomic integrity. Using heterozygous ATR-I774Yfs*5 HCT-116 cells to mimic the native mutation, we found this mutation reduced ATR activity as measured by damage-induced Chk1 phosphorylation at S317 and ATR autophosphorylation ATR at T1989. ATR-I774Yfs*5 expression impaired genomic stability as visualized by the appearance of micronuclei in two stable expression models as well as in cell lines transfected with ATR-I774Yfs*5. Micronucleus development was dependent on replication and independent of ATR copy number. ATR-I774Yfs*5 expression did not alter cellular viability, cell cycle progression, or replicative rate, suggesting this mutation is well-tolerated despite its destabilizing effect on the genome. Taken together, these data suggest that the ATR-I774Yfs*5, whose development is favored in the context of MMR deficiency, may represent an important driver of a mutator phenotype by promoting genomic instability.

cancer biology↗