Biology subjects

Seller, C. A.

Publications and source records attributed to Seller, C. A..

5 recordsLinked to original sources

bioRxiv2026

Morphological and biochemical evaluation of tolerance to water deficit identifies SlCLE9 as a novel regulator of drought stress

We performed a screening to evaluate the responses to water deficit before the flowering stage in a panel of 31 genotypes composed of one commercial hybrid, one wild species, multiple ex-PVP (vintage) lines, several commercial heirlooms from the Northeast USA, Mexican landraces from hot and humid environments and genome edited lines with altered flowering and inflorescence traits. We characterized 18 different morphological, physiological and biochemical traits to assess the response to 40% water deficit. We observed diverse morphological, physiological and biochemical responses across the 31 genotypes screened, suggesting the presence of useful variation for breeding for drought tolerance in cultivated tomato. Interestingly, some heirlooms exhibited superior performance under drought, suggesting they can be used as donors to discover novel genes involved in drought responses. Unexpectedly, we found mutants in SlCLE9, a paralog of the stem cell regulator SlCLV3 known to co-regulate meristem proliferation in tomato, exhibited enhanced drought tolerance. Notably, the slcle9 mutant also conferred drought tolerance when used as rootstock with grafted scions from our reference cultivar M82, suggesting SlCLE9 influence root architecture and drought response. Consistent with this, we found SlCLE9 is transcriptionally upregulated in roots and leaves during drought stress, and exogenous application of SlCLE9 modifies root growth and response to drought. Altogether, our screening uncovered new potential trait donors for breeding against drought stress and describes a novel role for SlCLE9 in drought tolerance.

plant biology↗

bioRxiv2023

Guard cell epigenomics reveals distinct abscisic acid and CO2 triggered chromatin remodeling during stomatal movements

In plants, epidermal guard cells integrate and respond to numerous environmental signals to control stomatal pore apertures thereby regulating gas exchange. Chromatin structure controls transcription factor access to the genome, but whether large-scale chromatin remodeling occurs in guard cells during stomatal movements, and in response to the hormone abscisic acid (ABA) in general, remain unknown. Here we isolate guard cell nuclei from Arabidopsis thaliana plants to examine whether the physiological signals, ABA and CO2, regulate guard cell chromatin during stomatal movements. Our cell type specific analyses uncover patterns of chromatin accessibility specific to guard cells and define novel cis-regulatory sequences supporting guard cell specific gene expression. We find that ABA triggers extensive and dynamic chromatin remodeling in guard cells, roots, and mesophyll cells with clear patterns of cell-type specificity. DNA motif analyses uncover binding sites for distinct transcription factors enriched in ABA-induced and ABA-repressed chromatin. We identify the ABF/AREB bZIP-type transcription factors that are required for ABA-triggered chromatin opening in guard cells and implicate the inhibition of a set of bHLH-type transcription factors in controlling ABA-repressed chromatin. Moreover, we demonstrate that ABA and CO2 induce distinct programs of chromatin remodeling. We provide insight into the control of guard cell chromatin dynamics and propose that ABA-induced chromatin remodeling primes the genome for abiotic stress resistance. Significance statementSpecialized leaf cells called guard cells integrate environmental cues to optimally control the size of microscopic stomatal pores. The hormone abscisic acid (ABA), a key regulator of plant drought responses, and changes in atmospheric CO2 concentration are signals that control stomatal aperture size, but whether these signals also regulate genome packaging into chromatin is unknown. Using guard cell specific chromatin profiling we uncovered regulatory DNA sequences driving specific gene expression in this cell-type. We also discovered that ABA triggers extensive and persistent changes to chromatin structure in guard cells. Unexpectedly, exposure of plants to elevated atmospheric CO2 had only minimal impact on chromatin dynamics. Furthermore, we identified the specific transcription factors that regulate ABA-induced chromatin dynamics in guard cells.

plant biology↗

bioRxiv2022

Temporal control of late replication and coordination of origin firing by self-stabilizing Rif1-PP1 hubs in Drosophila

In the metazoan S phase, coordinated firing of clusters of origins replicates different parts of the genome in a temporal program. Despite advances, neither the mechanism controlling timing nor that coordinating firing of multiple origins is fully understood. Rif1, an evolutionarily conserved inhibitor of DNA replication, recruits protein phosphatase 1 (PP1) and counteracts firing of origins by S-phase kinases. During the mid-blastula transition (MBT) in Drosophila embryos, Rif1 forms subnuclear hubs at each of the large blocks of satellite sequences and delays their replication. Each Rif1 hub disperses abruptly just prior to the replication of the associated satellite sequences. Here, we show that the level of activity of the S-phase kinase, DDK, accelerated this dispersal program, and that the level of Rif1-recruited PP1 retarded it. Further, Rif1-recruited PP1 supported chromatin association of nearby Rif1. This influence of nearby Rif1 can create a "community effect" counteracting kinase-induced dissociation such that an entire hub of Rif1 undergoes switch-like dispersal at characteristic times that shift in response to the balance of Rif1-PP1 and DDK activities. We propose a model in which the spatiotemporal program of late replication in the MBT embryo is controlled by self-stabilizing Rif1-PP1 hubs, whose abrupt dispersal synchronizes firing of associated late origins. SIGNIFICANCESeventy years ago, it was discovered that large domains of the eukaryotic genome replicate at different times. Detailed descriptions left significant questions unresolved. How are the many origins in the large domains coordinated to fire in unison? What distinguishes different domains and gives rise to a temporal program? When Drosophila embryos first establish late replication, an inhibitor of DNA replication, Rif1, forms hubs over domains of late replicating DNA. Rif1 recruits protein phosphatase 1 (PP1), which prevents kinases from dispersing Rif1 hubs or activating associated origins. When kinase activity eventually exceeds a hub-specific threshold, the self-stabilization of Rif1-PP1 breaks down, hubs disperse abruptly, and all associated origins are free to initiate.

cell biology↗

bioRxiv2018

Rapid embryonic cell cycles defer the establishment of heterochromatin by Eggless/SetDB1 in Drosophila

Acquisition of chromatin modifications during embryogenesis distinguishes different regions of an initially naive genome. In many organisms, repetitive DNA is packaged into constitutive heterochromatin that is marked by di/tri methylation of histone H3K9 and the associated protein HP1a. These modifications enforce the unique epigenetic properties of heterochromatin. However, in the early Drosophila melanogaster embryo the heterochromatin lacks these modifications which only appear later when rapid embryonic cell cycles slow down at the Mid-Blastula Transition or MBT. Here we focus on the initial steps restoring heterochromatic modifications in the embryo. We describe the JabbaTrap, a technique for inactivating maternally provided proteins in embryos. Using the JabbaTrap we reveal a major requirement for the methyltransferase Eggless/SetDB1 in the establishment of heterochromatin. In contrast, other methyltransferases contribute minimally. Live-imaging reveals that endogenous Eggless gradually accumulates on chromatin in interphase, but then dissociates in mitosis and its accumulation must restart in the next cell cycle. Cell cycle slowing as the embryo approaches the MBT permits increasing accumulation and action of Eggless at its targets. Experimental manipulation of interphase duration shows that cell cycle speed regulates Eggless. We propose that developmental slowing of the cell cycle times embryonic heterochromatin formation.

developmental biology↗

bioRxiv2017

Rif1 prolongs the embryonic S phase at the Drosophila mid-blastula transition

In preparation for dramatic morphogenetic events of gastrulation, rapid embryonic cell cycles slow at the Mid-Blastula Transition, MBT. In Drosophila melanogaster embryos, downregulation of Cdk1 activity initiates this slowing by delaying replication of satellite sequences and extending S phase. We found that Cdk1 inhibited the chromatin association of Rif1, a candidate repressor of replication. Furthermore, Rif1 bound selectively to satellite sequences following Cdk1 downregulation at the MBT. In the next S phase, Rif1 dissociated from different satellites in an orderly schedule that anticipated their replication. Rif1 lacking potential phosphorylation sites failed to dissociate and dominantly prevented completion of replication. Loss of Rif1 in mutant embryos shortened the post-MBT S phase, and rescued embryonic cell cycles disrupted by depletion of the S phase-promoting kinase, Cdc7. Thus, Drosophila Rif1 mediates the MBT extension of S phase and functionally interacts with S phase promoting kinases to introduce a replication-timing program.

developmental biology↗