bims-plasge 2020-09-13 papers

PeerJ. 2020 ;8 e9772

Plastid transit peptides-where do they come from and where do they all belong? Multi-genome and pan-genomic assessment of chloroplast transit peptide evolution.

Ryan W Christian, Seanna L Hewitt, Grant Nelson, Eric H Roalson, Amit Dhingra.

Subcellular relocalization of proteins determines an organism's metabolic repertoire and thereby its survival in unique evolutionary niches. In plants, the plastid and its various morphotypes import a large and varied number of nuclear-encoded proteins to orchestrate vital biochemical reactions in a spatiotemporal context. Recent comparative genomics analysis and high-throughput shotgun proteomics data indicate that there are a large number of plastid-targeted proteins that are either semi-conserved or non-conserved across different lineages. This implies that homologs are differentially targeted across different species, which is feasible only if proteins have gained or lost plastid targeting peptides during evolution. In this study, a broad, multi-genome analysis of 15 phylogenetically diverse genera and in-depth analyses of pangenomes from Arabidopsis and Brachypodium were performed to address the question of how proteins acquire or lose plastid targeting peptides. The analysis revealed that random insertions or deletions were the dominant mechanism by which novel transit peptides are gained by proteins. While gene duplication was not a strict requirement for the acquisition of novel subcellular targeting, 40% of novel plastid-targeted genes were found to be most closely related to a sequence within the same genome, and of these, 30.5% resulted from alternative transcription or translation initiation sites. Interestingly, analysis of the distribution of amino acids in the transit peptides of known and predicted chloroplast-targeted proteins revealed monocot and eudicot-specific preferences in residue distribution.

Keywords: Chloroplast; Multi-genome; Pangenome; Plastid; Protein targeting; Signal peptide; Transit peptide

DOI: https://doi.org/10.7717/peerj.9772

Plants (Basel). 2020 Sep 08. pii: E1163. [Epub ahead of print]9(9):

QTL Mapping and Candidate Gene Analysis for Pod Shattering Tolerance in Soybean (Glycine max).

Jeong-Hyun Seo, Beom-Kyu Kang, Sanjeev K Dhungana, Jae-Hyeon Oh, Man-Soo Choi, Ji-Hee Park, Sang-Ouk Shin, Hong-Sik Kim, In-Youl Baek, Jung-Sook Sung, Chan-Sik Jung, Ki-Seung Kim, Tae-Hwan Jun.

Pod shattering is an important reproductive process in many wild species. However, pod shattering at the maturing stage can result in severe yield loss. The objectives of this study were to discover quantitative trait loci (QTLs) for pod shattering using two recombinant inbred line (RIL) populations derived from an elite cultivar having pod shattering tolerance, namely "Daewonkong", and to predict novel candidate QTL/genes involved in pod shattering based on their allele patterns. We found several QTLs with more than 10% phenotypic variance explained (PVE) on seven different chromosomes and found a novel candidate QTL on chromosome 16 (qPS-DS16-1) from the allele patterns in the QTL region. Out of the 41 annotated genes in the QTL region, six were found to contain SNP (single-nucleotide polymorphism)/indel variations in the coding sequence of the parents compared to the soybean reference genome. Among the six potential candidate genes, Glyma.16g076600, one of the genes with known function, showed a highly differential expression levels between the tolerant and susceptible parents in the growth stages R3 to R6. Further, Glyma.16g076600 is a homolog of AT4G19230 in Arabidopsis, whose function is related to abscisic acid catabolism. The results provide useful information to understand the genetic mechanism of pod shattering and could be used for improving the efficiency of marker-assisted selection for developing varieties of soybeans tolerant to pod shattering.

Keywords: abscisic acid; candidate gene; pod shattering; quantitative trait loci; soybean

DOI: https://doi.org/10.3390/plants9091163

Curr Biol. 2020 Sep 03. pii: S0960-9822(20)31240-9. [Epub ahead of print]

A Peptide Pair Coordinates Regular Ovule Initiation Patterns with Seed Number and Fruit Size.

Nozomi Kawamoto, Dunia Pino Del Carpio, Alexander Hofmann, Yoko Mizuta, Daisuke Kurihara, Tetsuya Higashiyama, Naoyuki Uchida, Keiko U Torii, Lucia Colombo, Georg Groth, Rüdiger Simon.

Ovule development in Arabidopsis thaliana involves pattern formation, which ensures that ovules are regularly arranged in the pistils to reduce competition for nutrients and space. Mechanisms underlying pattern formation in plants, such as phyllotaxis, flower morphogenesis, or lateral root initiation, have been extensively studied, and genes controlling the initiation of ovules have been identified. However, the fundamental patterning mechanism that determines the spacing of ovule anlagen within the placenta remained unexplored. Using natural variation analysis combined with quantitative trait locus analysis, we found that the spacing of ovules in the developing gynoecium and fruits is controlled by two secreted peptides, EPFL2 and EPFL9 (also known as Stomagen), and their receptors from the ERECTA (ER) family that act from the carpel wall and the placental tissue. We found that a signaling pathway controlled by EPFL9 acting from the carpel wall through the LRR-receptor kinases ER, ERL1, and ERL2 promotes fruit growth. Regular spacing of ovules depends on EPFL2 expression in the carpel wall and in the inter-ovule spaces, where it acts through ERL1 and ERL2. Loss of EPFL2 signaling results in shorter gynoecia and fruits and irregular spacing of ovules or even ovule twinning. We propose that the EPFL2 signaling module evolved to control the initiation and regular, equidistant spacing of ovule primordia, which may serve to minimize competition between seeds or facilitate equal resource allocation. Together, EPFL2 and EPFL9 help to coordinate ovule patterning and thereby seed number with gynoecium and fruit growth through a set of shared receptors.

Keywords: Arabidopsis; EPFL2; EPFL9; ERfamily receptor kinases; ovules; pattern formation

DOI: https://doi.org/10.1016/j.cub.2020.08.050