HKT channels are a plant protein family involved in sodium (Na⁺) and potassium (K⁺) uptake and Na⁺-K⁺ homeostasis. Some HKTs underlie salt tolerance responses in plants, while others provide a mechanism to cope with short-term K⁺ shortage by allowing increased Na⁺ uptake under K⁺ starvation conditions. HKT channels present a functionally versatile family divided into two classes, mainly based on a sequence polymorphism found in the sequences underlying the selectivity filter of the first pore loop. Physiologically, most class I members function as sodium uniporters, and class II members as Na⁺/K⁺ symporters. Nevertheless, even within these two classes, there is a high functional diversity that, to date, cannot be explained at the molecular level. The high complexity is also reflected at the regulatory level. HKT expression is modulated at the level of transcription, translation, and functionality of the protein. Here, we summarize and discuss the structure and conservation of the HKT channel family from algae to angiosperms. We also outline the latest findings on gene expression and the regulation of HKT channels.

In arbuscular mycorrhizal (AM) symbiosis, fungi and plants exchange nutrients (sugars and phosphate, for instance) for reciprocal benefit. Until now it is not clear how this nutrient exchange system works. Here, we used computational cell biology to simulate the dynamics of a network of proton pumps and proton-coupled transporters that are upregulated during AM formation. We show that this minimal network is sufficient to describe accurately and realistically the nutrient trade system. By applying basic principles of microeconomics, we link the biophysics of transmembrane nutrient transport with the ecology of organismic interactions and straightforwardly explain macroscopic scenarios of the relations between plant and AM fungus. This computational cell biology study allows drawing far reaching hypotheses about the mechanism and the regulation of nutrient exchange and proposes that the ‘cooperation’ between plant and fungus can be in fact the result of a competition between both for the same resources in the tiny periarbuscular space. The minimal model presented here may serve as benchmark to evaluate in future the performance of more complex models of AM nutrient exchange. As a first step towards this goal, we included SWEET sugar transporters in the model and show that their co-occurrence with proton-coupled sugar transporters results in a futile carbon cycle at the plant plasma membrane proposing that two different pathways for the same substrate should not be active at the same time.

Two-pore domain potassium (K_2P) channels are membrane proteins widely identified in mammals, plants, and other organisms. A functional channel is a dimer with each subunit comprising two pore-forming loops and four transmembrane domains. The genome of the model plant Arabidopsis thaliana harbors five genes coding for K_2P channels. Homologs of Arabidopsis K_2P channels have been found in all higher plants sequenced so far. As with the K_2P channels in mammals, plant K_2P channels are targets of external and internal stimuli, which fine-tune the electrical properties of the membrane for specialized transport and/or signaling tasks. Plant K_2P channels are modulated by signaling molecules such as intracellular H⁺ and calcium and physical factors like temperature and pressure. In this review, we ask the following: What are the similarities and differences between K_2P channels in plants and animals in terms of their physiology? What is the nature of the last common ancestor (LCA) of these two groups of proteins? To answer these questions, we present physiological, structural, and phylogenetic evidence that discards the hypothesis proposing that the duplication and fusion that gave rise to the K_2P channels occurred in a prokaryote LCA. Conversely, we argue that the K_2P LCA was most likely a eukaryote organism. Consideration of plant and animal K_2P channels in the same study is novel and likely to stimulate further exchange of ideas between students of these fields.

In recent years, Transposable Elements (TEs) have been related to gene regulation. However, estimating the origin of expression of TEs through RNA-seq is complicated by multi-mapping reads coming from their repetitive sequences. Current approaches that address multi-mapping reads are focused in expression quantification and not in finding the origin of expression. Addressing the genomic origin of expressed TEs could further aid in understanding the role that TEs might have in the cell. We have developed a new pipeline called TEcandidates, based on de novo transcriptome assembly to assess the instances of TEs being expressed, along with their location, to include in downstream DE analysis. TEcandidates takes as input the RNA-seq data, the genome sequence and the TE annotation file and returns a list of coordinates of candidate TEs being expressed, the TEs that have been removed and the genome sequence with removed TEs as masked. This masked genome is suited to include TEs in downstream expression analysis, as the ambiguity of reads coming from TEs is significantly reduced in the mapping step of the analysis. The script which runs the pipeline can be downloaded at http://www.mobilomics.org/tecandidates/downloads or http://github.com/TEcandidates/TEcandidates. Supplementary data are available at Bioinformatics online.

Transposable Elements (TEs) are ubiquitous genetic elements with the ability to move within a genome. TEs contribute to a large fraction of the repetitive elements of a genome, and because of their nature, they are not routinely analyzed in RNA-Seq gene expression studies. Amyotrophic Lateral Sclerosis (ALS) is a lethal neurodegenerative disease, and a well-accepted model for its study is the mouse harboring the human SOD1^G93A mutant. In this model, landmark stages of the disease can be recapitulated at specific time points, making possible to understand changes in gene expression across time. While there are several works reporting TE activity in ALS models, they have not explored their activity through the disease progression. Moreover, they have done it at the expense of losing their locus of expression. Depending on their genomic location, TEs can regulate genes in cis and in trans, making locus-specific analysis of TEs of importance in order to understand their role in modulating gene expression. Particularly, the locus-specific role of TEs in ALS has not been fully elucidated. In this work, we analyzed publicly available RNA-Seq datasets of the SOD1^G93A mouse model, to understand the locus-specific role of TEs. We show that TEs become up-regulated at the early stages of the disease, and via statistical associations, we speculate that they can regulate several genes, which in turn might be contributing to the genetic dysfunction observed in ALS.