Development Of Control Research Articles

Dendritic cells in developing and adult zebrafish arise from different origins and display distinct flt3 dependencies.

Dendritic cells (DCs) are key cellular components of the immune system and perform critical functions in innate and acquired immunity. In mammals, it is generally believed that DCs originate exclusively from hematopoietic stem cells (HSCs). Using a temporal-spatial resolved fate-mapping system, here we show that in zebrafish, DCs arise from two sources: dorsal aorta-born endothelium-derived hematopoietic progenitors (EHPs) and HSCs. The EHP-derived DCs emerge early, predominantly colonizing the developing thymus during larval stages and diminishing by juvenile stages. In contrast, HSC-derived DCs emerge later and can populate different tissues from late larval stages to adulthood. We further document that the EHP- and HSC-derived DCs display different dependencies on Fms-like tyrosine kinase 3 (Flt3), a pivotal receptor tyrosine kinase crucial for DC development in mammals. Our study reveals the presence of two distinct waves of DC development in zebrafish, each with unique origins and developmental controls.

MEDIATOR15 destabilizes DELLA protein to promote gibberellin-mediated plant development.

Mediator, a transcriptional coactivator, regulates plant growth and development by interacting with various transcriptional regulators. MEDIATOR15 (MED15) is a subunit in the Mediator complex potentially involved in developmental control. To uncover molecular functions of Arabidopsis MED15 in development, we searched for its interactors. MED15 was found to interact with DELLA proteins, which negatively regulate gibberellic acid (GA) signaling and positively regulate GA biosynthesis. Mutants and overexpressors of MED15 exhibited multiple GA-related growth phenotypes, which resembled the phenotypes of the DELLA overexpressor and mutant, respectively. Consistent with this observation, DELLA protein levels were inversely correlated with MED15 protein levels, suggesting that MED15 activates GA signaling through DELLA degradation. MED15 was required not only for DELLA-mediated induction of GA-biosynthesis gene expression but also for GA-mediated degradation of DELLA. Therefore, MED15 facilitates DELLA destruction not only by promoting GA biosynthesis but also by accelerating DELLA turnover. Furthermore, MED15-mediated GA signaling was required for timely developmental responses to dark and warm conditions. Our results provide insight into developmental control by Mediator via precise regulation of DELLA stability. These findings are potentially useful for the generation of new crop cultivars with ideal body architecture.

Multiple Elevation‐Dependent Climate Signals From Quantitative Wood Anatomical Measurements of Rocky Mountain Bristlecone Pine

AbstractSouthwestern North America has experienced significant temperature increases over the last century, leading to intensified droughts that significantly affect montane forests. Although tree‐ring data have provided long‐term context for this recent drought severity, the varying physiological responses of trees to climate variability make it challenging to disentangle the combined influence of temperature and soil moisture. Here we investigate complex climate‐growth relationships in Rocky Mountain bristlecone pine (Pinus aristata) at a low‐elevation and a high‐elevation site using quantitative wood anatomy (QWA). Significant correlations with climate were found for low‐elevation tree‐ring width (TRW) and earlywood chronologies, including positive correlations with spring and early summer precipitation and drought indices and negative correlations with spring and early summer maximum temperatures. At high elevations, TRW and earlywood chronologies show positive responses to summer moisture, whereas latewood chronologies correlate positively with August and September maximum temperatures and negatively with August precipitation. We leverage this differing seasonality of moisture and temperature signals and compare the QWA data to known droughts. The earlywood lumen area is found to be highly responsive to drought because of its physiological reliance on water availability for maintaining turgor pressure during cell enlargement. We also observed a decline in temperature sensitivity at the high elevation site, suggesting shifts in the dominance of limiting factors. Integrating QWA with traditional dendrochronology improves interpretations of tree‐ring data for use in climate reconstruction, offering detailed insights into tree physiological responses and the mix of environmental and developmental controls on cell growth.

Association between epigenome-wide DNA methylation changes and early neurodevelopment in preschool children: Evidence from a former impoverished county in Central China.

Existing epigenome-wide association study (EWAS) investigating the association between DNA methylation (DNAm) and child neurodevelopment have been predominantly conducted within Western populations, and yielded inconsistent results, leading to a significant gap within non-Western setting, particularly in resource-limited rural areas of Central China. To investigate the association between altered epigenome-wide DNAm and neurodevelopment in preschool children from resource-limited rural areas of Central China. This case-control study involved 64 preschoolers. We assessed children's neurodevelopment using the Gesell Developmental Diagnostic Scale. The neurodevelopmental potential was expressed as a global developmental quotient (DQ) score. We conducted an EWAS with an Illumina Infinium MethylationEPIC v1.0 BeadChip array, using blood samples from 32 suspected developmental delay children (DQ scores < 85) and 32 controls (DQ scores ≥ 85). Differentially methylated probes (DMPs) and differentially methylated regions (DMRs) between the suspected developmental delay and control groups were analyzed. Multivariate linear regression models were used to evaluate the association between global DQ scores and DNAm. Functional enrichment analyses were conducted using Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG). The BECon tool was utilized to estimate the concordance of CpGs between blood and the human brain. A total of 66 DMRs (PFDR < 0.05) were identified between the two groups, but no DMPs were found. After FDR correction, 844 methylated CpG sites exhibited significant associations with the global DQ scores in children. Genes annotated by methylated CpGs were enriched in the "oxytocin signaling pathway", "mTOR signaling pathway", and "thyroid hormone signaling pathway". They were also involved in the "regulation of cell development", "cell-cell junction", and "ATPase activity". Among the top 20 CpGs, nine global DQ scores related-CpGs had blood-brain DNA methylation correlations, and six CpGs among them had an absolute Spearman correlation coefficient bigger than 0.2. Preschoolers from a former impoverished county exhibited epigenome-wide DNAm changes strongly linked to early neurodevelopment. This study enhances our understanding of the epigenetic landscape associated with early neurodevelopment, and suggests the potential for developmenting epigenetic biomarkers that could facilitate the early identification of children at a higher risk of compromised neurodevelopment, as well as holding implication to inform novel interventions, especially in underprivileged regions.

Dual regulation of stomatal development by brassinosteroid in Arabidopsis hypocotyls.

Stomata are epidermal pores that are essential for water evaporation and gas exchange in plants. Stomatal development is orchestrated by intrinsic developmental programs, hormonal controls, and environmental cues. The steroid hormone brassinosteroid (BR) inhibits stomatal lineage progression by regulating BIN2 and BSL proteins in leaves. Notably, BR is known to promote stomatal development in hypocotyls as opposed to leaves; however, its molecular mechanism remains elusive. Here, we show that BR signaling has a dual regulatory role in controlling stomatal development in Arabidopsis hypocotyls. We found that brassinolide (BL; the most active BR) regulates stomatal development differently in a concentration-dependent manner. At low and moderate concentrations, BL promoted stomatal formation by upregulating the expression of SPEECHLESS (SPCH) and its target genes independently of BIN2 regulation. In contrast, high concentrations of BL and bikinin, which is a specific inhibitor of BIN2 and its homologs, significantly reduced stomatal formation. Genetic analyses revealed that BIN2 regulates stomatal development in hypocotyls through molecular mechanisms distinct from the regulatory mechanism of the cotyledons. In hypocotyls, BIN2 promoted stomatal development by inactivating BZR1, which suppresses the expression of SPCH and its target genes. Taken together, our results suggest that BR precisely coordinates the stomatal development of hypocotyls using an antagonistic control of SPCH expression via BZR1-dependent and BZR1-independent transcriptional regulation.

Altered Temporospatial Variability of Dynamic Amplitude of Low-Frequency Fluctuation in Children with Autism Spectrum Disorder.

Autism spectrum disorder (ASD) is a neurodevelopmental disorder with altered brain activity. However, little is known about the integrated temporospatial variation of dynamic spontaneous brain activity in ASD. In the present study, resting-state functional magnetic resonance imaging data were analyzed for 105 ASD and 102 demographically-matched typically developmental controls (TC) children obtained from the Autism Brain Imaging Data Exchange database. Using the sliding-window approach, temporal, spatial, and temporospatial variability of dynamic amplitude of low-frequency fluctuation (tvALFF, svALFF, and tsvALFF) were calculated for each participant. Group-comparisons were further performed at global, network, and brain region levels to quantify differences between ASD and TC groups. The relationship between temporospatial dynamic amplitude of low-frequency fluctuation variation alterations and clinical symptoms of ASD was finally explored by a support vector regression model. Relative to TC, we found enhanced tvALFF in visual network (Vis), somatomotor network (SMT), and salience/ventral attention network (SVA) of ASD, and weakened tvALFF in dorsal attention network (DAN) of ASD. Besides, ASD showed decreased svALFF in Vis, SVA, and limbic network (Limbic), and increased svALFF in DAN and default mode network (DMN). Elevated tsvALFF was found in the Vis, SMT, and DMN of ASD. More importantly, the altered tsvALFF from the DMN can predict the symptom severity of ASD. These findings demonstrate altered temporospatial dynamics of the spontaneous brain activity in ASD and provide novel insights into the neural mechanism underlying ASD.

Developmental control of rod number via a light-dependent retrograde pathway from intrinsically photosensitive retinal ganglion cells.

Photoreception is essential for the development of the visual system, shaping vision's first synapse to cortical development. Here, we find that the lighting environment controls developmental rod apoptosis via Opn4-expressing intrinsically photosensitive retinal ganglion cells (ipRGCs). Using genetics, sensory environment manipulations, and computational approaches, we establish a pathway where light-dependent glutamate released from ipRGCs is detected via a transiently expressed glutamate receptor (Grik3) on rod precursors within the inner retina. Communication between these cells is mediated by hybrid neurites on ipRGCs that sense light before eye opening. These structures span the ipRGC-rod precursor distance over development and contain the machinery for photoreception (Opn4) and neurotransmitter release (Vglut2& Syp). Assessment of the human gestational retina identifies conserved hallmarks of an ipRGC-to-rod axis, including displaced rod precursors, transient GRIK3 expression, and ipRGCs with deep-projecting neurites. This analysis defines an adaptive retrograde pathway linking the sensory environment to rod precursors via ipRGCs prior to eye opening.

Modeling Functional Brain Networks for ADHD via Spatial Preservation-Based Neural Architecture Search.

Modeling functional brain networks (FBNs) for attention deficit hyperactivity disorder (ADHD) has sparked significant interest since the abnormal functional connectivity is discovered in certain functional magnetic resonance imaging (fMRI)-based brain regions compared to typical developmental control (TC) individuals. However, existing models for modeling FBNs generally use dimensionality reduction techniques to process the high dimensional input data, which results in confusion and an inaccurate representation of voxel interactions between spatially close brain regions, causing misdiagnosis of the disease. To address these issues, we propose a spatial preservation-based neural architecture search (SP-NAS) for FBNs modeling in ADHD. The main work includes three-fold: 1) A spatial preservation module is designed to embed original spatial information into dimensionality reduction data, addressing the challenge of a large number of parameters in the original data and mitigating disease misdiagnosis resulting from voxel confusion between different brain regions caused by dimensionality reduction. 2) A search space using more suitable search operations is constructed to efficiently extract spatial-temporal interaction characteristics of fMRI data in ADHD while narrowing the search space. 3) Cross-regional association differences between ADHD and TC groups are explored for ADHD auxiliary diagnosis since the abnormal activation regions of ADHD relative to TC on the brain regions and the abnormal connectivity between the lesion brain regions are identified. Model validation results on the ADHD-200 dataset show that the FBNs obtained from SP-NAS not only achieve competitive results in ADHD diagnosis but also reveal abnormal connections in the lesion regions of ADHD consistent with clinical diagnosis.

The global phosphorylation landscape of mouse oocytes during meiotic maturation.

Phosphorylation is a key post-translational modification regulating protein function and biological outcomes. However, the phosphorylation dynamics orchestrating mammalian oocyte development remains poorly understood. In the present study, we apply high-resolution mass spectrometry-based phosphoproteomics to obtain the first global in vivo quantification of mouse oocyte phosphorylation. Of more than 8000 phosphosites, 75% significantly oscillate and 64% exhibit marked upregulation during meiotic maturation, indicative of the dominant regulatory role. Moreover, we identify numerous novel phosphosites on oocyte proteins and a few highly conserved phosphosites in oocytes from different species. Through functional perturbations, we demonstrate that phosphorylation status of specific sites participates in modulating critical events including metabolism, translation, and RNA processing during meiosis. Finally, we combine inhibitor screening and enzyme-substrate network prediction to discover previously unexplored kinases and phosphatases that are essential for oocyte maturation. In sum, our data define landscape of the oocyte phosphoproteome, enabling in-depth mechanistic insights into developmental control of germ cells.

Ancient developmental genes underlie evolutionary novelties in walking fish

A critical question in biology is how new traits evolve, but studying this in wild animals remains challenging. Here, we probe the genetic basis of trait gain in sea robin fish, which have evolved specialized leg-like appendages for locomotion and digging along the ocean floor. We use genome sequencing, transcriptional profiling, and interspecific hybrid analysis to explore the molecular and developmental basis of leg formation. We identified the ancient, conserved transcription factor tbx3a as a major determinant of sensory leg development. Genome editing confirms that tbx3a is required for normal leg formation in sea robins, and for formation of enlarged central nervous system lobes, sensory papillae, and adult digging behavior. Our study establishes sea robins as a model organism for studying the evolution of major trait gain and illustrates how ancient developmental control genes can underlie novel organ formation.

Identification of the genetic determinants of shovel-shaped incisors and Carabelli’s cusp

Shovel-shaped incisors (SSI) and Carabelli’s cusp (CC) are noteworthy human dental non-metric traits which presence and degree of expression have been reported to cluster within distinct populations. Recent advances in developmental biology suggest that SSI and CC are likely under polygenic developmental control; therefore, genetic variation in multiple genes is likely to contribute to differential SSI and CC expression. The exact genetic mechanisms underlying variation in SSI and CC development, however, remain mostly unknown. This study aims to identify whether variation in the basal DNA sequences of six candidate genes, NKX2-3, SOSTDC1, BMP4, FGF3, FGF4, and WNT10A, has any impact on SSI and/or CC expression. Study methods involve collection of saliva samples and dental data from 36 participants. The Arizona State University Dental Anthropology System (ASUDAS) has been used to score SSI and CC expression. Next-generation sequencing (NGS) methods were utilized to sequence the entire gene region of the candidate genes. Spearman’s correlation test was used to score the relationship between the genotype and degree of trait expression of participants. Fifteen SNPs/INDELs belonging to SOSTDC1, FGF3, FGF4 and WNT10A were significantly associated with SSI and/or CC expression. No SNPs/INDELs were detected in the genes BMP4 and NKX2-3 that significantly contributes to observed phenotypes. FGF3, FGF4, SOSTDC1 and WNT10A were possibly involved in the formation of shoveling and Carabelli’s cusp. However, because of the small sample size, more studies are needed to confirm their role and rule out any potential role of NKX2-3 and BMP4 in the production of SSI and CC.

Developmental characteristics and control effects of myopia and eye diseases in children and adolescents: a school-based retrospective cohort study in Southwest China

ObjectivesTo characterise the prevalence of myopia and eye diseases among school adolescents and children in Southwest China, and to evaluate the effectiveness of myopia control tools.DesignRetrospective cohort study.SettingAcross 95 basic...

Senescence-Associated Sugar Transporter1 affects developmental master regulators and controls senescence in Arabidopsis.

Sugar transport across membranes is critical for plant development and yield. However, an analysis of the role of intracellular sugar transporters in senescence is lacking. Here, we characterized the role of Senescence-Associated Sugar Transporter1 (SAST1) during senescence in Arabidopsis (Arabidopsis thaliana). SAST1 expression was induced in leaves during senescence and after the application of abscisic acid (ABA). SAST1 is a vacuolar protein that pumps glucose out of the cytosol. sast1 mutants exhibited a stay-green phenotype during developmental senescence, after the darkening of single leaves, and after ABA feeding. To explain the stay-green phenotype of sast1 mutants, we analyzed the activity of the glucose-induced master regulator TOR (target of rapamycin), which is responsible for maintaining a high anabolic state. TOR activity was higher in sast1 mutants during senescence compared to wild types, whereas the activity of its antagonist, SNF1-related protein kinase 1 (SnRK1), was reduced in sast1 mutants under senescent conditions. This deregulation of TOR and SnRK1 activities correlated with high cytosolic glucose levels under senescent conditions in sast1 mutants. Although sast1 mutants displayed a functional stay-green phenotype, their seed yield was reduced. These analyses place the activity of SAST1 in the last phase of a leaf's existence in the molecular program required to complete its life cycle.

KREH2 helicase represses ND7 mRNA editing in procyclic-stage Trypanosoma brucei by opposite modulation of canonical and 'moonlighting' gRNA utilization creating a proposed mRNA structure.

Unknown factors regulate mitochondrial U-insertion/deletion (U-indel) RNA editing in procyclic-form (PCF) and bloodstream-form (BSF) T. brucei. This editing, directed by anti-sense gRNAs, creates canonical protein-encoding mRNAs and may developmentally control respiration. Canonical editing by gRNAs that specify protein-encoding mRNA sequences occurs amid massive non-canonical editing of unclear sources and biological significance. We found PCF-specific repression at a major early checkpoint in mRNA ND7, involving helicase KREH2-dependent opposite modulation of canonical and non-canonical 'terminator' gRNA utilization. Terminator-programmed editing derails canonical editing and installs proposed repressive structure in 30% of the ND7 transcriptome. BSF-to-PCF differentiation in vitro recreated this negative control. Remarkably, KREH2-RNAi knockdown relieved repression and increased editing progression by reverting canonical/terminator gRNA utilization. ND7 transcripts lacking early terminator-directed editing in PCF exhibited similar negative editing control along the mRNA sequence, suggesting global modulation of gRNA utilization fidelity. The terminator is a 'moonlighting' gRNA also associated with mRNA COX3 canonical editing, so the gRNA transcriptome seems multifunctional. Thus, KREH2 is the first identified repressor in developmental editing control. This and our prior work support a model whereby KREH2 activates or represses editing in a stage and substrate-specific manner. KREH2's novel dual role tunes mitochondrial gene expression in either direction during development.

Genetic mechanisms of axial patterning in Apeltes quadracus.

The genetic mechanisms underlying striking axial patterning changes in wild species are still largely unknown. Previous studies have shown that Apeltes quadracus fish, commonly known as fourspine sticklebacks, have evolved multiple different axial patterns in wild populations. Here, we revisit classic locations in Nova Scotia, Canada, where both high-spined and low-spined morphs are particularly common. Using genetic crosses and quantitative trait locus (QTL) mapping, we examine the genetic architecture of wild differences in several axial patterning traits, including the number and length of prominent dorsal spines, the number of underlying median support bones (pterygiophores), and the number and ratio of abdominal and caudal vertebrae along the anterior-posterior body axis. Our studies identify a highly significant QTL on chromosome 6 that controls a substantial fraction of phenotypic variation in multiple dorsal spine and pterygiophore traits (~15%-30% variance explained). An additional smaller-effect QTL on chromosome 14 contributes to the lengths of both the last dorsal spine and anal spine (~9% variance explained). 1 or no QTL were detected for differences in the numbers of abdominal and caudal vertebrae. The major-effect patterning QTL on chromosome 6 is centered on the HOXDB gene cluster, where sequence changes in a noncoding axial regulatory enhancer have previously been associated with prominent dorsal spine differences in Apeltes. The QTL that have the largest effects on dorsal spine number and length traits map to different chromosomes in Apeltes and Gasterosteus, 2 distantly related stickleback genera. However, in both genera, the major-effect QTL for prominent skeletal changes in wild populations maps to linked clusters of powerful developmental control genes. This study, therefore, bolsters the body of evidence that regulatory changes in developmental gene clusters provide a common genetic mechanism for evolving major morphological changes in natural species.

Life stage–specific poly(A) site selection regulated by Trypanosoma brucei DRBD18

The kinetoplastid parasite, Trypanosoma brucei, undergoes a complex life cycle entailing slender and stumpy bloodstream forms in mammals and procyclic and metacyclic forms (MFs) in tsetse fly hosts. The numerous gene regulatory events that underlie T. brucei differentiation between hosts, as well as between active and quiescent stages within each host, take place in the near absence of transcriptional control. Rather, differentiation is controlled by RNA-binding proteins (RBPs) that associate with mRNA 3' untranslated regions (3'UTRs) to impact RNA stability and translational efficiency. DRBD18 is a multifunctional T. brucei RBP, shown to impact mRNA stability, translation, export, and processing. Here, we use single-cell RNAseq to characterize transcriptomic changes in cell populations that arise upon DRBD18 depletion, as well as to visualize transcriptome-wide alterations to 3'UTR length. We show that in procyclic insect stages, DRBD18 represses expression of stumpy bloodstream form and MF transcripts. Additionally, DRBD18 regulates the 3'UTR lengths of over 1,500 transcripts, typically promoting the use of distal polyadenylation sites, and thus the inclusion of 3'UTR regulatory elements. Remarkably, comparison of polyadenylation patterns in DRBD18 knockdowns with polyadenylation patterns in stumpy bloodstream forms shows numerous similarities, revealing a role for poly(A) site selection in developmental gene regulation, and indicating that DRBD18 controls this process for a set of transcripts. RNA immunoprecipitation supports a direct role for DRBD18 in poly(A) site selection. This report highlights the importance of alternative polyadenylation in T. brucei developmental control and identifies a critical RBP in this process.

Essential function of transmembrane transcription factor MYRF in promoting transcription of miRNA lin-4 during C. elegans development.

Precise developmental timing control is essential for organism formation and function, but its mechanisms are unclear. In C. elegans, the microRNA lin-4 critically regulates developmental timing by post-transcriptionally downregulating the larval-stage-fate controller LIN-14. However, the mechanisms triggering the activation of lin-4 expression toward the end of the first larval stage remain unknown. We demonstrate that the transmembrane transcription factor MYRF-1 is necessary for lin-4 activation. MYRF-1 is initially localized on the cell membrane, and its increased cleavage and nuclear accumulation coincide with lin-4 expression timing. MYRF-1 regulates lin-4 expression cell-autonomously and hyperactive MYRF-1 can prematurely drive lin-4 expression in embryos and young first-stage larvae. The tandem lin-4 promoter DNA recruits MYRF-1GFP to form visible loci in the nucleus, suggesting that MYRF-1 directly binds to the lin-4 promoter. Our findings identify a crucial link in understanding developmental timing regulation and establish MYRF-1 as a key regulator of lin-4 expression.

Methylome analysis in girls with idiopathic central precocious puberty

BackgroundGenetic and environmental factors are implicated in many developmental processes. Recent evidence, however, has suggested that epigenetic changes may also influence the onset of puberty or the susceptibility to a wide range of diseases later in life. The present study aims to investigate changes in genomic DNA methylation profiles associated with pubertal onset analyzing human peripheral blood leukocytes from three different groups of subjects: 19 girls with central precocious puberty (CPP), 14 healthy prepubertal girls matched by age and 13 healthy pubertal girls matched by pubertal stage. For this purpose, the comparisons were performed between pre- and pubertal controls to identify changes in normal pubertal transition and CPP versus pre- and pubertal controls.ResultsAnalysis of methylation changes associated with normal pubertal transition identified 1006 differentially methylated CpG sites, 86% of them were found to be hypermethylated in prepubertal controls. Some of these CpG sites reside in genes associated with the age of menarche or transcription factors involved in the process of pubertal development. Analysis of methylome profiles in CPP patients showed 65% and 55% hypomethylated CpG sites compared with prepubertal and pubertal controls, respectively. In addition, interestingly, our results revealed the presence of 43 differentially methylated genes coding for zinc finger (ZNF) proteins. Gene ontology and IPA analysis performed in the three groups studied revealed significant enrichment of them in some pathways related to neuronal communication (semaphorin and gustation pathways), estrogens action, some cancers (particularly breast and ovarian) or metabolism (particularly sirtuin).ConclusionsThe different methylation profiles of girls with normal and precocious puberty indicate that regulation of the pubertal process in humans is associated with specific epigenetic changes. Differentially methylated genes include ZNF genes that may play a role in developmental control. In addition, our data highlight changes in the methylation status of genes involved in signaling pathways that determine the migration and function of GnRH neurons and the onset of metabolic and neoplastic diseases that may be associated with CPP in later life.

Developmental Control of Cell Cycle and Signaling

Developmental Control of Cell Cycle and Signaling

Plastid dynamism integrates development and environment

In land plants plastid type differentiation occurs concomitantly with cellular differentiation and the transition from one type to another is under developmental and environmental control. Plastid dynamism is based on a bilateral communication between plastids and nucleus through anterograde and retrograde signaling. Signaling occurs through the interaction with specific phytohormones (abscisic acid, strigolactones, jasmonates, gibberellins, brassinosteroids, ethylene, salicylic acid, cytokinin and auxin). The review is focused on the modulation of plastid capabilities at both transcriptional and post-translational levels at the crossroad between development and stress, with a particular attention to the chloroplast, because the most studied plastid type. The role of plastid-encoded and nuclear-encoded proteins for plastid development and stress responses, and the changes of plastid fate through the activity of stromules and plastoglobules, are discussed. Examples of plastid dynamism in response to soil stress agents (salinity, lead, cadmium, arsenic, and chromium) are described. Albinism and root greening are described based on the modulation activities of auxin and cytokinin. The physiological and functional responses of the sensory epidermal and vascular plastids to abiotic and biotic stresses along with their specific roles in stress sensing are described together with their potential modulation of retrograde signaling pathways. Future research perspectives include an in-depth study of sensory plastids to explore their potential for establishing a transgenerational memory to stress. Suggestions about anterograde and retrograde pathways acting at interspecific level and on the lipids of plastoglobules as a novel class of plastid morphogenic agents are provided.