Identification of a New Giant Emrbryo Allele, and Integrated Transcriptomics and Metabolomics Analysis of Giant Embryo Development in Rice

Rice embryos are rich in high-quality protein, lipid, vitamins and minerals, representing the most important nutritional part of brown rice. However, the molecular mechanism of rice embryo development is poorly understood. In this study, two rice cultivars with contrasting embryo size (the giant embryo cultivar Dapeimi and the normal embryo cultivar 187R) were used to explore excellent genes controlling embryo size, and the developed near-isogenic lines (NILs) (NIL-D, which has the giant embryo phenotype, and its matching line, NIL-X) were used to explore transcript and metabolic properties in the earlier maturation stage of giant embryo development under natural conditions. The map-based cloning results demonstrated that Dapeimi is a novel allelic mutant of the rice GIANT EMBRYO (GE) gene, and the functional mutation site is a single cytosine deletion in the exon1. A total of 285 differentially accumulated metabolites (DAMs) and 677 differentially expressed genes (DEGs) were identified between NIL-D and NIL-X. The analysis of DAMs indicated that plants lacking GE mainly promoted energy metabolism, amino acid metabolism, and lipid metabolism pathways in the rice embryo. Pearson correlation coefficient showed that 300 pairs of gene-metabolites were highly correlated. Among them, OsZS_02G0528500 and OsZS_12G0013700 were considered to be key genes regulating L-Aspartic acid and L-Tryptophan content during rice giant embryo development, which are promising to be good candidate genes to improve rice nutrition. By analyzing rice embryo development through a combination of strategies, this research contributes to a greater understanding of the molecular mechanism of rice embryo development, and provides a theoretical foundation for breeding high-nutrition varieties.

Scaling dictates the decoder structure

Despite variability in embryo size, the tissue, organ and body plan developin proportionwith embryo size, known as the scaling phenomenon. Scale-invariant patterning of gene expression is a common feature in development and regeneration, and can be generated by mechanisms such as scaling morphogen gradient and dynamic oscillation. However, whether and how static non-scaling morphogens (input) can induce a scaling gene expression (output) across the entire embryo is not clear. Here we show that scaling requirement sets severe constraints on the geometric structure of the input-output relation (the decoder), from which information about the regulation and mutants’ behavior can be deduced without going into any molecular details. We demonstrate that theDrosophilagap gene system achieves scaling in the way that is entirely consistent with our theory. Remarkably, following the geometry dictated by scaling, a parameter-free decoder correctly and quantitatively accounts for the gap gene expression patterns in nearly all morphogen mutants. Furthermore, the regulation logic and the coding/decoding strategy of the gap gene system can also be revealed from the decoder geometry. Our work provides a general theoretical framework on a large class of problems where scaling output is induced by non-scaling input, as well as a unified understanding of scaling, mutants’ behavior and regulation in theDrosophilagap gene and related systems.Significance StatementWithin a given species, fluctuation in egg or embryo size is unavoidable. Despite this, the gene expression pattern and hence the embryonic structure often scale in proportion with the body length. Thisscalingphenomenon is very common in development and regeneration, and has long fascinated scientists. In this paper, the authors address the question of whether and how a scaling gene expression pattern can originate from non-scaling signals (morphogens). They found that scaling has profound implications in the developmental programming -- properties and behaviors of the underlying gene network can be deduced from the scaling requirement. They demonstrated that the scaling in fruit fly embryogenesis indeed works in this way. Thus, although biological regulatory systems are very complex in general, it can be forced to exhibit simple macroscopic behaviors due to selection pressure, as demonstrated in this study.

What Drives Life-History Variation in the Livebearing Fish Poeciliopsis prolifica? An Assessment of Multiple Putative Selective Agents

Life-history traits are directly linked to fitness, and therefore, can be highly adaptive. Livebearers have been used as models for understanding the evolution of life histories due to their wide diversity in these traits. Several different selective pressures, including population density, predation, and resource levels, can shape life-history traits. However, these selective pressures are usually considered independently in livebearers and we lack a clear understanding of how they interact in shaping life-history evolution. Furthermore, selective pressures such as interspecific competition are rarely considered as drivers of life-history evolution in poeciliids. Here we test the simultaneous effects of several potential selective pressures on life-history traits in the livebearing fish Poeciliopsis prolifica. We employ a multi-model inference approach. We focus on four known agents of selection: resource availability, stream velocity, population density, and interspecific competition, and their effect on four life-history traits: reproductive allocation, superfetation, number of embryos, and individual embryo size. We found that models with population density and interspecific competition alone were strongly supported in our data and, hence, indicated that these two factors are the most important selective agents for most life-history traits, except for embryo size. When population density and interspecific competition increase there is an increase in each of the three life-history traits (reproductive allocation, superfetation, and number of embryos). For individual embryo size, we found that all single-agent models were equivalent and it was unclear which selective agent best explained variation. We also found that models that included population density and interspecific competition as direct effects were better supported than those that included them as indirect effects through their influence on resource availability. Our study underscores the importance of interspecific competitive interactions on shaping life-history traits and suggests that these interactions should be considered in future life-history studies.

Scaling of Internal Organs during Drosophila Embryonic Development

Many species show a diverse range of sizes; for example, domestic dogs have large variation in body mass. Yet, the internal structure of the organism remains similar, i.e. the system scales to organism size. Drosophila melanogaster has been a powerful model system for exploring scaling mechanisms. In the early embryo, gene expression boundaries scale very precisely to embryo length. Later in development, the adult wings grow with remarkable symmetry and scale well with animal size. Yet, our knowledge of whether internal organs initially scale to embryo size remains largely unknown. Here, we utilise artificially small Drosophila embryos to explore how three critical internal organs - the heart, hindgut and ventral nerve cord (VNC) - adapt to changes in embryo morphology. We find that the heart scales precisely with embryo length. Intriguingly, reduction in cardiac cell length, rather than number, appears to be important in controlling heart length. The hindgut - which is the first chiral organ to form - displays scaling with embryo size under large-scale changes in the artificially smaller embryos but shows few hallmarks of scaling within wild-type size variation. Finally, the VNC only displays weak scaling behaviour; even large changes in embryo geometry result in only small shifts in VNC length. This suggests that the VNC may have an intrinsic minimal length, which is largely independent of embryo length. Overall, our work shows that internal organs can adapt to embryo size changes in Drosophila. but the extent to which they scale varies significantly between organs.