Biology subjects

Qiu, Y.

Publications and source records attributed to Qiu, Y..

At least 19 recordsLinked to original sources

bioRxiv2018

The mitochondrial DNA content can not predict the embryo viability

ObjectiveTo investigate whether the mitochondrial DNA content could predict the embryo viability\n\nDesignRetrospective analysis.\n\nSettingReproductive genetics laboratory\n\nPatient(s)A total of 421 biopsied samples obtained from 129 patients\n\nIntervention(s)Embryo biopsies samples underwent whole genome amplification (WGA) and were tested by next generation sequencing (NGS) and array Comparative Genomic Hybridization (aCGH), 30 samples were selected randomly to undergo quantitative real-time polymerase chain reaction (qPCR).\n\nMain Outcome Measure(s)Those embryos which obtained the consistent chromosome status determined both aCGH and NGS platform were further classified. We investigated the relationship of mtDNA content with several factors including female patient age, embryo morphology, chromosome status, and live birth rate of both blastocysts and blastomeres.\n\nResult(s)A total of 386 (110 blastomeres and 276 blastocysts) out of 399 embryos showed consistent chromosome status outcome. We found no statistically difference was observed in aneuploid and euploid blastocysts (p=0.14), the same phenomenon was observed in aneuploid and euploid blastomeres (p=0.89). Similarly, the mtDNA content was independent of female patient age, embryo morphology and live birth rate.\n\nConclusion(s)The mtDNA content did not provide a reliable prediction of the viability of blastocysts to initiate a pregnancy.

ecology↗

bioRxiv2018

CRISPRa-mediated Kcna1 upregulation decreases neuronal excitability and suppresses seizures in a rodent model of temporal lobe epilepsy

Epilepsy is a major health burden, calling for new mechanistic and therapeutic insights. CRISPR-mediated gene editing shows promise to cure genetic pathologies, although hitherto it has mostly been applied ex-vivo. Its translational potential for treating non-genetic pathologies is still unexplored. Furthermore, neurological diseases represent an important challenge for the application of CRISPR, because of the need in many cases to manipulate gene function of neurons in situ. A variant of CRISPR, CRISPRa, offers the possibility to modulate the expression of endogenous genes by directly targeting their promoters. We asked if this strategy can effectively treat acquired focal epilepsy, focusing on ion channels because their manipulation is known be effective in changing network hyperactivity and hypersynchronisation. We applied a doxycycline-inducible CRISPRa technology to increase the expression of the potassium channel gene Kcna1 (encoding Kv1.1) in mouse hippocampal excitatory neurons. CRISPRa-mediated Kv1.1 upregulation led to a substantial decrease in neuronal excitability. Continuous video-EEG telemetry showed that AAV9-mediated delivery of CRISPRa, upon doxycycline administration, decreased spontaneous generalized tonic-clonic seizures in a model of temporal lobe epilepsy, and rescued cognitive impairment and transcriptomic alterations associated with chronic epilepsy. The focal treatment minimizes concerns about off-target effects in other organs and brain areas. This study provides the proof of principle for a translational CRISPR-based approach to treat neurological diseases characterized by abnormal circuit excitability.

neuroscience↗

bioRxiv2018

MdMYB3 helps regulate anthocyanin accumulation in apple calli under moderately acidic conditions

Anthocyanins are the key factors controlling the coloration of plant tissues. However, the molecular mechanism underlying the effects of environmental pH on the synthesis of apple anthocyanins is unclear. In this study, we analyzed the anthocyanin contents of apple calli cultured in media at different pHs (5.5, 6.0, and 6.5). The highest anthocyanin content was observed at pH 6.0. Additionally, the moderately acidic conditions up-regulated the expression of MdMYB3 as well as specific anthocyanin biosynthesis structural genes (MdDFR and MdUFGT). Moreover, the anthocyanin content was higher in calli overexpressing MdMYB3 than in the wild-type controls at different pHs. Yeast one-hybrid assay results indicated that MdMYB3 binds to the MdDFR and MdUFGT promoters in vivo. An analysis of the MdDFR and MdUFGT promoters revealed multiple MYB-binding sites. Meanwhile, electrophoretic mobility shift assays confirmed that MdMYB3 binds to the MdDFR and MdUFGT promoters in vitro. Furthermore, GUS promoter activity assays suggested that the MdDFR and MdUFGT promoter activities are enhanced by acidic conditions, and the binding of MdMYB3 may further enhance activity. These results implied that an acid-induced apple MYB transcription factor (MdMYB3) promotes anthocyanin accumulation by up-regulating the expression of MdDFR and MdUFGT under moderately acidic conditions.

molecular biology↗

bioRxiv2018

Dietary fatty acids promote lipid droplet diversity through seipin enrichment in an ER subdomain

Exogenous metabolites from microbial and dietary origins have profound effects on host metabolism. Here, we report that a sub-population of lipid droplets (LDs), which are conserved organelles for fat storage, is defined by metabolites-driven targeting of the C. elegans seipin ortholog, SEIP-1. Loss of SEIP-1 function reduced the size of a subset of LDs while over-expression of SEIP-1 had the opposite effect. Ultrastructural analysis revealed SEIP-1 enrichment in an endoplasmic reticulum (ER) subdomain, which co-purified with LDs. Analyses of C. elegans and bacterial genetic mutants indicated a requirement of polyunsaturated fatty acids (PUFAs) and microbial cyclopropane fatty acids (CFAs) for SEIP-1 enrichment, as confirmed by dietary supplementation experiments. In mammalian cells, heterologous expression of SEIP-1 promoted lipid droplet expansion from ER subdomains in a conserved manner. Our results suggest that microbial and polyunsaturated fatty acids serve unexpected roles in regulating cellular fat storage by enforcing LD diversity.

cell biology↗

bioRxiv2018

The genetics and genome-wide screening of perennialism loci in Zea diploperennis

Perennialism is common among the higher plants, yet we know little about its inheritance. To address this, six hybrids were made by reciprocally crossing perennial Zea diploperennis Iltis, Doebley & R. Guzman with three varieties/inbred lines of annual maize (Z. mays L. spp. mays). We specifically focused on the plants ability to regrow after flowering and senescence. All the F1 plants demonstrated senescence and regrowth for several cycles, indicating a dominant effect of the Z. diploperennis alleles. The regrowth ability was stably transmitted to progeny of the hybrids in segregation ratios that suggested the trait was controlled by two dominant, complementary loci. Genome-wide screening with genotyping-by-sequencing (GBS) identified two major regrowth loci reg1 and reg2 on chromosomes 2 and 7, respectively. GBS results were validated using a larger F2 population and PCR markers derived from the single nucleotide polymorphisms within the locus intervals. These markers will be employed to select near-isogenic lines for the two loci and to identify candidate genes in the loci in Z. diploperennis.\n\nSignificance StatementOur study contributes to our general understanding of inheritance of perennialism in the higher plants. Previous genetic studies of the perennialism in Zea have yielded contradictory results. We take a reductionist approach by specifically focusing on the plants ability to regenerate new shoots after senescence without regard to associated traits, such as rhizome formation, tillering or environmental impacts. Using this criterion, inheritance of perennialism in Zea appears to be dominantly and qualitatively inherited. Importantly, our data indicate that there is no major barrier to transferring this trait into maize or other grass crops for perennial crop development, which enhances sustainability of grain crop production in an environmentally friendly way.

plant biology↗

bioRxiv2018

Glucose signaling is important for nutrient adaptation during differentiation of pleomorphic African trypanosomes

The African trypanosome has evolved mechanisms to adapt to changes in nutrient availability that occur during its lifecycle. During transition from mammalian blood to insect vector gut, parasites experience a rapid reduction in environmental glucose. Here we describe how pleomorphic parasites respond to glucose depletion with a focus on parasite changes in energy metabolism and growth. Long slender bloodstream form parasites are rapidly killed as glucose concentrations fall, while the short stumpy bloodstream form parasites persist to differentiate into the insect stage procyclic form parasite. The rate of differentiation was slower than that triggered by other cues but reached physiological rates when combined with cold shock. Both differentiation and growth of resulting procyclic form parasites were inhibited by glucose and its non-metabolizable analogs in a concentration dependent manner. Procyclic form parasites differentiated from short stumpy form parasites in glucose depleted medium significantly upregulated gene expression of amino acid metabolic pathway components when compared to procyclic forms generated by cis-aconitate treatment. Additionally, growth of these parasite was inhibited by the presence of either glucose or 6-deoxyglucose. In summary, glucose transitions from the primary metabolite of the blood stage infection to a negative regulator of cell development and growth in the insect vector, suggesting that the hexose is not only a key metabolic agent but is also an important signaling molecule.\n\nAuthor SummaryAs the African trypanosome, Trypanosoma brucei, completes its lifecycle, it encounters many different environments. Adaptation to these environments includes modulation of metabolic pathways to parallel the availability of nutrients. Here, we describe how the blood-dwelling lifecycle stages of the African trypanosome, which consume glucose to meet their nutritional needs, respond differently to culture in the near absence of glucose. The proliferative long slender parasites rapidly die, while the non-dividing short stumpy remains viable and undergoes differentiation to the next lifecycle stage, the procyclic form parasite. Interestingly a sugar analog that cannot be used as an energy source inhibited the process. Furthermore, the growth of procyclic form parasite that resulted from the event was inhibited by glucose, a behavior that is similar to that of parasites isolated from tsetse flies. Our findings suggest that glucose sensing serves as an important modulator of nutrient adaptation in the parasite.

microbiology↗

bioRxiv2018

Identification of a post-transcriptional regulatory element that responds to glucose in the African trypanosome

The ability to adapt to varying nutrient availability in changing environments is critical for successful parasitism. The lifecycle stages of the African trypanosome, Trypanosoma brucei, that infect the host mammalian bloodstream utilize glucose exclusively for ATP production. The finding that trypanosomes also inhabit other tissues that frequently contain lower glucose concentrations suggests blood stage parasites may have to respond to a dynamic environment with changing nutrient availability in order to survive. However, little is known about how the parasites coordinate gene expression with nutrient availability. Through transcriptome analysis, we have found blood stage parasites deprived of glucose alter gene expression in a pattern similar to transcriptome changes triggered by other stresses. A surprisingly low concentration of glucose (<10 M) was required to initiate the response. To further understand the dynamic regulation of gene expression that occurs in response to altered glucose availability in the environment, we have interrogated the 3UTR of cytochrome c oxidase subunit VI, a known lifecycle stage regulated gene, and have identified a stem-loop structure that confers glucose-responsive regulation at the translational level.

genetics↗

bioRxiv2018

Pancreatic islet chromatin accessibility and conformation defines distal enhancer networks of type 2 diabetes risk

The gene targets of enhancer activity in pancreatic islets are largely unknown, impeding discovery of islet regulatory networks involved in type 2 diabetes (T2D) risk. We mapped chromatin state, accessibility and conformation using ChIP-seq, ATAC-seq and Hi-C in human pancreatic islets, which we integrated with T2D genetic fine-mapping and islet expression QTL data. Active islet regulatory elements preferentially interacted with other active elements, often at distances over 1MB, and we identified target genes for thousands of distal islet enhancers. A third of T2D risk signals mapped in islet enhancers, and target genes regulated by these signals were specifically involved in processes related to protein transport and secretion. Among implicated target genes of T2D islet enhancer signals with no prior known role in islet function, we demonstrated that reduced IGF2BP2 activity in mouse islets leads to impaired glucose-stimulated insulin secretion. These results link distal islet enhancer regulation of protein secretion and transport to genetic risk of T2D, and highlight the utility of high-throughput chromatin conformation maps to uncover the gene regulatory networks of complex disease.

genomics↗

bioRxiv2018

Co-regulation of alternative splicing by hnRNPM and ESRP1 during EMT

The epithelial-mesenchymal transition (EMT) is a fundamental developmental process that is abnormally activated in cancer metastasis. Dynamic changes in alternative splicing occur during EMT. ESRP1 and hnRNPM are splicing regulators that promote an epithelial splicing program and a mesenchymal splicing program, respectively. The functional relationships between these splicing factors in the genome-scale remain elusive. Comparing alternative splicing targets of hnRNPM and ESRP1 revealed that they co-regulate a set of cassette exon events, with the majority showing discordant splicing regulation. hnRNPM discordantly regulated splicing events show a positive correlation with splicing during EMT while concordant splicing events do not, highlighting the antagonistic role of hnRNPM and ESRP1 during EMT. Motif enrichment analysis near co-regulated exons identifies guanine-uridine rich motifs downstream of hnRNPM-repressed and ESRP1-enhanced exons, supporting a model of competitive binding to these cis-elements to antagonize alternative splicing. The set of co-regulated exons are enriched in genes associated with cell-migration and cytoskeletal reorganization, which are pathways associated with EMT. Splicing levels of co-regulated exons are associated with breast cancer patient survival and correlate with gene sets involved in EMT and breast cancer subtypes. These data identify complex modes of interaction between hnRNPM and ESRP1 in regulation of splicing in disease-relevant contexts.

molecular biology↗

bioRxiv2018

ADS-J1 Disaggregates Semen-derived Amyloid Fibrils

Semen-derived amyloid fibrils, composing SEVI (semen-derived enhancer of viral infection) fibrils and SEM1 fibrils, could remarkably enhance HIV-1 sexual transmission and thus, are potential targets for the development of an effective microbicide. Previously, we found that ADS-J1, apart from being an HIV-1 entry inhibitor, could also potently inhibit seminal amyloid fibrillization and block fibril-mediated enhancement of viral infection. However, the remodeling effects of ADS-J1 on mature seminal fibrils were unexplored. Herein, we investigated the capacity of ADS-J1 to disassemble seminal fibrils and the potential mode of action by applying several biophysical and biochemical measurements, combined with molecular dynamic (MD) simulations. We found that ADS-J1 effectively remodeled SEVI, SEM186-107 fibrils and endogenous seminal fibrils. Unlike epi-gallocatechin gallate (EGCG), a universal amyloid fibril breaker, ADS-J1 disaggregated SEVI fibrils into monomeric peptides, which was independent of oxidation reaction. MD simulations revealed that ADS-J1 displayed strong binding potency to the full-length PAP248-286 via electrostatic interactions, hydrophobic interactions and hydrogen bonds. ADS-J1 might initially bind to the fibrillar surface and then occupy the amyloid core, which eventually lead to fibril disassembly. Furthermore, the binding of ADS-J1 with PAP248-286 might induce conformational changes of PAP248-286. Disassembled PAP248-286 might not be favor to re-aggregate into fibrils. ADS-J1 also exerts abilities to remodel a panel of amyloid fibrils, including A{beta}1-42, hIAPP1-37 and EP2 fibrils. ADS-J1 displays promising potential to be a combination microbicide and an effective lead-product to treat amyloidogenic diseases.

pharmacology and toxicology↗

bioRxiv2018

Highly efficient CRISPR/Cas9-mediated tissue specific mutagenesis in Drosophila

Tissue-specific loss-of-function (LOF) analysis is an essential approach for characterizing gene function. Here we describe an efficient CRISPR-mediated tissue-restricted mutagenesis (CRISPR-TRiM) method for ablating gene function in Drosophila. This binary system consists of a tissue-specific Cas9 and a ubiquitously expressed multi-guide RNA (gRNA) transgene. To facilitate the construction of these components, we developed convenient tools for generating and evaluating enhancer-driven Cas9 lines, identified a multi-gRNA design that is highly efficient in mutagenizing somatic cells, and established an assay for testing the efficiency of multi-gRNAs in creating double-stranded breaks. We found that excision of genomic DNA induced by two gRNAs is infrequent in somatic cells, while indels more reliably cause tissue-specific LOF. Furthermore, we show that enhancer-driven Cas9 is less cytotoxic yet results in more complete gene removal than Gal4-driven Cas9 in larval neurons. Finally, we demonstrate that CRISPR-TRiM efficiently unmasks redundant gene functions in neuronal morphogenesis. Importantly, two Cas9 transgenes that turn on with different timings in the neuronal lineage revealed the extent to which gene products persist in cells after tissue-specific gene knockout. These CRISRPR tools can be applied to analyze tissue-specific gene function in many biological processes.

developmental biology↗

bioRxiv2017

Removing unwanted variation between samples in Hi-C experiments

Hi-C data is commonly normalized using single sample processing methods, with focus on comparisons between regions within a given contact map. Here, we aim to compare contact maps across different samples. We demonstrate that unwanted variation, of likely technical origin, is present in Hi-C data with replicates from different individuals, and that properties of this unwanted variation changes across the contact map. We present BNBC, a method for normalization and batch correction of Hi-C data and show that it substantially improves comparisons across samples, including in a QTL analysis as well as differential enrichment across cell types.

genomics↗

bioRxiv2017

Exchange protein directly activated by cAMP plays a critical role in regulation of vascular fibrinolysis

RationaleTo maintain vascular patency, endothelial cells (ECs) actively regulate hemostasis. Among the myriad of pathways by which they control both fibrin formation and fibrinolysis is EC expression of annexin A2 (ANXA2) in a heterotetrameric complex with S100A10 [(ANXA2-S100A10)2]. This complex is a well-recognized endothelial surface platform for the activation of plasminogen by tissue plasminogen activator. A noteworthy advance in this field came about when it was shown that the cAMP pathway is linked to the regulation of (ANXA2-S100A10)2 in ECs.\n\nObjectiveThese findings prompted us to determine whether a druggable target, namely the exchange protein directly activated by cAMP (EPAC) pathway, plays a role in vascular luminal fibrinolysis.\n\nMethods and ResultsTaking advantage of our Epac1-null mouse model, we found that depletion of Epac1 results in fibrin deposition, fibrinolytic dysfunction, and decreased endothelial surface ANXA2 in mice, which are similar to phenomena discovered in ANXA2-null and S100A10-null mice. We observed upregulation of EPAC1 and downregulation of fibrin in endocardial tissues beneath atrial mural thrombi in humans. Of note, our thrombosis model revealed that dysfunction of fibrinolysis in EPAC1-null mice can be ameliorated by recombinant ANXA2. Furthermore, we demonstrated that suppression of EPAC1 using a small-molecule inhibitor (ESI09) reduces the expression of ANXA2 in lipid rafts and impedes ANXA2 association with S100A10. Endothelial apical surface expression of both ANXA2 and S100A10 were markedly decreased in ESI09-treated ECs, which was corroborated by results from a nanoforce spectroscopy study. Moreover, inactivation of EPAC1 decreases tyrosine 23 phosphorylation of ANXA2 in the cell membrane compartment.\n\nConclusionsOur data reveal a novel role for EPAC1 in vascular fibrinolysis, by showing that EPAC1 is responsible for the translocation of ANXA2 to the EC surface. This process promotes conversion of plasminogen to plasmin, thereby enhancing local fibrinolytic activity.

cell biology↗

bioRxiv2017

Functional Modeling of Plant Growth Dynamics

Recent advances in automated plant phenotyping have enabled the collection time series measurements from the same plants of a wide range of traits over different developmental time scales. The availability of time series phenotypic datasets has increased interest in statistical approaches for comparing patterns of change between different plant genotypes and different treatment conditions. Two widely used methods of modeling growth over time are point-wise analysis of variance (ANOVA) and parametric sigmoidal curve fitting. Point-wise ANOVA yields discontinuous growth curves, which do not reflect the true dynamics of growth patterns in plants. In contrast, fitting a parametric model to a time series of observations does capture the trend of growth, however these models require assumptions regarding the true pattern of plant growth. Depending on the species, treatment regime, and subset of the plant lifecycle sampled this assumptions will not always hold true. Here we introduce a different approach - functional ANOVA - which yields continuous growth curves without requiring assumptions regarding patterns of plant growth. We compare and validate this approach using data from an experiment measuring growth of two maize (Zea mays ssp. mays) genotypes under two water availability treatments over a 21-day period. Functional ANOVA enables a nonparametric estimation of the dynamics of changes in plant traits over time without assumptions regarding curve shape. In addition to estimating smooth curves of trait values over time, functional ANOVA also estimates the the derivatives of these curves - e.g. growth rates - simultaneously. Using two different subsampling strategies, we demonstrate that this functional ANOVA method enables the comparison of growth curves between plants phenotyped on non-overlapping days with little reduction in estimation accuracy. This means functional ANOVA based approaches can allow larger numbers of samples and biological replicates to be scored in a single experiment given fixed amounts of phenotyping infrastructure and personnel.

plant biology↗

bioRxiv2017

Conventional and hyperspectral time-series imagingof maize lines widely used in field trials

Maize (Zea mays ssp. mays) is one of three crops, along with rice and wheat, responsible for more than 1/2 of all calories consumed around the world. Increasing the yield and stress tolerance of these crops is essential to meet the growing need for food. The cost and speed of plant phenotyping is currently the largest constraint on plant breeding efforts. Datasets linking new types of high throughput phenotyping data collected from plants to the performance of the same genotypes under agronomic conditions across a wide range of environments are essential for developing new statistical approaches and computer vision based tools. A set of maize inbreds - primarily recently off patent lines - were phenotyped using a high throughput platform at University of Nebraska-Lincoln. These lines have been previously subjected to high density genotyping, and scored for a core set of 13 phenotypes in field trials across 13 North American states in two years by the Genomes to Fields consortium. A total of 485 GB of image data including RGB, hyperspectral, fluorescence and thermal infrared photos has been released. Correlations between image-based measurements and manual measurements demonstrated the feasibility of quantifying variation in plant architecture using image data. However, naive approaches to measuring traits such as biomass can introduce nonrandom measurement errors confounded with genotype variation. Analysis of hyperspectral image data demonstrated unique signatures from stem tissue. Integrating heritable phenotypes from high-throughput phenotyping data with field data from different environments can reveal previously unknown factors influencing yield plasticity.

plant biology↗

bioRxiv2017

Systematic mapping of chromatin state landscapes during mouse development

Embryogenesis requires epigenetic information that allows each cell to respond appropriately to developmental cues. Histone modifications are core components of a cells epigenome, giving rise to chromatin states that modulate genome function. Here, we systematically profile histone modifications in a diverse panel of mouse tissues at 8 developmental stages from 10.5 days post conception until birth, performing a total of 1,128 ChIP-seq assays across 72 distinct tissue-stages. We combine these histone modification profiles into a unified set of chromatin state annotations, and track their activity across developmental time and space. Through integrative analysis we identify dynamic enhancers, reveal key transcriptional regulators, and characterize the role of chromatin-based repression in developmental gene regulation. We also leverage these data to link enhancers to putative target genes, revealing connections between coding and non-coding sequence variation in disease etiology. Our study provides a compendium of resources for biomedical researchers, and achieves the most comprehensive view of embryonic chromatin states to date.

genomics↗

bioRxiv2017

Mapping Human Hematopoietic Hierarchy At Single Cell Resolution By Microwell-seq

The classical hematopoietic hierarchy, which is mainly built with fluorescence-activated cell sorting (FACS) technology, proves to be inaccurate in recent studies. Single cell RNA-seq (scRNA-seq) analysis provides a solution to overcome the limit of FACS-based cell type definition system for the dissection of complex cellular hierarchy. However, large-scale scRNA-seq is constrained by the throughput and cost of traditional methods. Here, we developed Microwell-seq, a high-throughput and low-cost scRNA-seq platform using extremely simple devices. Using Microwell-seq, we constructed a single-cell resolution transcriptome atlas of human hematopoietic differentiation hierarchy by profiling more than 50,000 single cells throughout adult human hematopoietic system. We found that adult human hematopoietic stem and progenitor cell (HSPC) compartment is dominated by progenitors primed with lineage specific regulators. Our analysis revealed differentiation pathways for each cell types, through which HSPCs directly progress to lineage biased progenitors before differentiation. We propose a revised adult human hematopoietic hierarchy independent of oligopotent progenitors. Our study also demonstrates the broad applicability of Microwell-seq technology.

cell biology↗

bioRxiv2017

Differentially regulated ortholog analysis demonstrations that early transcriptional responses to cold have diverged slowly than downstream responses in panicoid grasses

Cross-species comparisons of transcriptional regulation have the potential to identify functionally constrained transcriptional regulation and genes for which a change in transcriptional regulation correlates with a change in phenotype. Conventional differential gene expression analysis and a different approach based on identifying differentially regulated orthologs (DROs) are compared using paired time course gene expression data from two species which respond similarly to cold - maize (Zea mays) and sorghum (Sorghum bicolor). Both approaches suggest that, for genes conserved at syntenic positions for millions of years, the majority of cold responsive transcriptional regulation is species specific, although initial transcriptional responses to cold appear to be more conserved between the two species than later responses. In maize, the promoters of genes with both species specific and conserved transcriptional responses to cold tend to contain more micrococcal nuclease hypersensitive sites in their promoters, a proxy for open chromatin. However, genes with conserved patterns of transcriptional regulation between the two species show lower ratios of nonsynonymous to synonymous substitutions consistent with this population of genes experiencing stronger purifying selection. We hypothesize that cold responsive transcriptional regulation is a fast evolving and largely neutral molecular phenotype for the majority of genes in Andropogoneae, while a smaller core set of genes involved in perceiving and responding to cold stress are subject to functionally constrained cold responsive regulation.

genetics↗