Biology subjects

Sancho-Andres, G.

Publications and source records attributed to Sancho-Andres, G..

4 recordsLinked to original sources

bioRxiv2026

Non-coding DNA dictates cell size and impairs fitness by sequestering RNA polymerase

Genome size varies greatly between organisms, largely because of varying amounts of non-coding DNA. In multicellular organisms, non-coding DNA can make up 99% of the genome, while unicellular organisms have little non-coding information. How non-coding DNA affects cell physiology remains a key question in understanding genome evolution. Here, we developed a system to conditionally accumulate large amounts of non-coding DNA in budding yeast cells. We show that cells adjust their size to DNA content, regardless of its coding capacity. The direct coupling of cell size to DNA content occurs independently of the known cell size control and DNA damage checkpoints and explains the long-observed correlation between cell size, genome size, and ploidy. Furthermore, we find that excess non-functional DNA compromises cell fitness and renders them hypersensitive to transcription inhibitors. Providing a potential explanation for this observation, we uncover that the transcription machinery binds non-coding DNA and is titrated away from coding genes, resulting in a reduced overall concentration of yeast transcripts. We propose that the inability of yeast to repress non-coding DNA increases the fitness cost associated with non-functional DNA and prevents its expansion in the yeast genome on evolutionary timescales.

cell biology↗

bioRxiv2026

The Receptor Kinase MEE39/ATHE Mediates Cell Wall Integrity Surveillance During Root Vascular Pathogen Infection

Plant cell wall (CW) integrity signaling enables early detection of microbial invasion, yet the receptors involved and their spatial and temporal dynamics during infection remain largely unknown. We identify ATHENA (ATHE)/MEE39, a previously uncharacterized malectin-like leucin-rich repeat receptor kinase (Mal-LRR-RK) that contributes to defense against the root vascular pathogen Fusarium oxysporum (Fo), particularly in outer root layers where colonization begins. ATHE abundance, localization, and endocytic trafficking are rapidly remodeled during infection, and loss of ATHE compromises basal immunity and early pathogen-induced transcriptional reprogramming. ATHE responds to altered cellulose synthesis, cellulose-derived oligosaccharides, mechanically induced CW perturbations, and the fungal secreted peptide Fo-RALF. In most of these contexts, ATHE acts together with the LRR-RK MIK2, forming a pathogen-strengthened RK complex that fine-tunes root responses to Fo. This represents the first example of a receptor complex visualized subcellularly in vivo during a plant-microbe interaction. Although Brassicaceae-specific, heterologous expression of ATHE enhanced tomato resistance to Fo, highlighting its functional relevance across plant lineages and its potential use for crop engineering. Our work reveals a previously unrecognized strategy by which plants decode microbial threats through dynamic CW-integrity surveillance.

plant biology↗

bioRxiv2022

A phospho-switch provided by LRR receptor-like kinase, ALK1/QSK1/KIN7, prioritizes ABCG36/PEN3/PDR8 transport toward defense

Based on its proposed substrate preferences, the ABC transporter, ABCG36/PDR8/PEN3, from the model plant Arabidopsis stands at the cross-road between growth and defence. Recently, ABCG36 was shown to export a few indolic compounds, including the auxin precursor, indole-3-butyric acid (IBA), and to be implicated in the export of the major phytoalexin of Arabidopsis, camalexin, although clear-cut proof of camalexin transport activity is still lacking. Here we provide strong evidence that ABCG36 catalyses the direct, ATP-dependent export of camalexin over the plasma membrane, however, most likely in functional interplay with non-camalexin transporting ABCG isoforms. We identify the leucin-rich repeat receptor-like kinase, Auxin-induced LRR Kinase1 (ALK1/KIN7/QSK1), as a functional kinase to physically interact with and phosphorylate ABCG36. ABCG36 phosphorylation by ALK1 represses unilaterally IBA but not camalexin export leading to a prioritization of ABCG transport toward defense. As a consequence, phospho-dead mutants of ABCG36, like alk1 and abcg36 alleles, are hypersensitive toward infection with the root pathogen, F. oxysporum, caused by elevated fungal progression. Our findings indicate a novel, direct regulatory circuit between a receptor kinase and an ABC transporter determining transporter substrate specificity. It appears that growth and defense balance decisions in plants are performed on the transporter level by means of a reversible phospho-switch.

plant biology↗

bioRxiv2021

Impairment of the cellulose degradation machinery enhances fungal virulence but limits reproductive fitness

Fungal endophytes grow in the apoplastic space, in constant contact with the plant cell wall (CW) that hinders microbe progression, while representing a source of nutrients. Although numerous fungal CW modifying proteins have been identified, their role during host colonization remains underexplored. Here we show that the root-infecting plant pathogen Fusarium oxysporum (Fo) does not require its complete arsenal of cellulases to infect the host plant. Quite the opposite, Fo mutants impaired in cellulose degradation become hypervirulent by enhancing the secretion of virulence factors. On the other hand, the reduction on cellulase activity had a severe negative effect on saprophytic growth and microconidia production during the final stages of the Fo infection cycle. These findings enhance our understanding on the function of plant CW degradation on the outcome of host-microbe interactions and reveal an unexpected role of cellulose degradation in a pathogens evolutionary success. TeaserUnexpectedly, fungi compromised in their capacity to degrade plant cellulose are hypervirulent but impaired in sporulation.

microbiology↗