Biology subjects

Kumari, K.

Publications and source records attributed to Kumari, K..

At least 19 recordsLinked to original sources

bioRxiv2026

Tvp38/DedA Family Protein mediates biogenesis of chloroplast peripheral reticulum and envelope-to-thylakoid contacts in Arabidopsis

Chloroplasts of land plants are dynamic organelles essential for photosynthesis, metabolism, and plant adaptation to changing environmental conditions. Within chloroplasts, the inner envelope and thylakoid membranes are spatially separated but functionally interconnected. The inner envelope harbors enzymes involved in lipid synthesis for internal membranes and controls the exchange of metabolites and proteins, whereas the thylakoid membranes accommodate the machinery of the photosynthetic electron transport chain responsible for converting light energy into chemical energy. Therefore, efficient communication between these membrane systems is essential for maintaining chloroplast homeostasis and sustaining photosynthetic activity. In this study we have characterized the role of Tvp38/DedA Family Protein (TVPFP) in mediating inner envelope-to-thylakoid communication in Arabidopsis thaliana. Despite exhibiting wild-type-like growth and similar accumulation of the major thylakoid-anchored photosynthetic complexes, tvpfp mutants displayed reduced photosynthetic activity and increased abundance of photorespiration- and pigment-related proteins. Our results revealed that TVPFP localizes to the chloroplast envelope and undergoes post-translational modification when localized to the thylakoids. The unmodified form of TVPFP is enriched in high-molecular-weight complexes, suggesting that TVPFP oligomers are partially dissolved upon thylakoid relocation. Transmission electron microscopy data showed reduced abundance of vesicles as well as chloroplast peripheral reticulum (CPR) structures connecting the envelope and thylakoids in tvpfp mutants. Together, our results demonstrate that TVPFP fine-tunes photosynthesis by regulating vesicle abundance and biogenesis of CPR structures. Our findings shed light on the importance of envelope-to-thylakoid communication and the role of CPR structures in land plants.

plant biology↗

bioRxiv2026

Molecular Mechanism of Lipid Recognition and Membrane-Guided Gating in Plant Minimal START Proteins

The hydrophobic nature of lipids requires specialized transport mechanisms, and one such non-vesicular transport mechanism involves START (StAR-related lipid transfer) domain proteins. START domains either occur as a part of multidomain proteins or occur solo as in minimal START proteins. Unlike well-studied multidomain variants, plant minimal START proteins remain poorly understood, leaving their ligand specificity, structural dynamics, and biological roles largely uncharacterized. Integrating structural screening with experimental validation, we analyzed representative plant minimal START proteins and confirmed their specific binding to amphipathic lipids, primarily myristic acid and lysophosphatidylcholine. The ligand binding involves a bipartite mechanism, in which basic residues within the cavity interact with polar lipid headgroups, while the hydrophobic tails are accommodated deeper within the cavity. Mechanistically, ligand binding induced closure of a lid-like gate at the cavity entrance, whereas membrane proximity promoted reopening of the gate and ligand release, collectively suggesting a membrane-guided gating mechanism for lipid exchange. Consistent with this model, localization studies show that these proteins associate with the endoplasmic reticulum, plastids, Golgi apparatus, and plasma membrane, major sites of lipid metabolism. Together, our findings establish plant minimal START proteins as bona fide lipid-binding proteins that utilize a bipartite ligand-binding mechanism coupled with membrane-responsive gating dynamics.

biochemistry↗

bioRxiv2026

Characterization of Chromatin-Associated Circular RNAs (cacRNAs)

HighlightsO_LIIdentified hundreds of potential chromatin-associated circRNAs in HEK293 cells, H9, and HeLa cells C_LIO_LIThe first report suggesting global interaction of circular RNAs with chromatin C_LIO_LIChromatin-associated circular RNAs interact with various RBPs involved in RNA splicing or processing C_LI Circular RNAs (circRNAs) have emerged as novel regulators of gene expression by interacting with various proteins and RNAs in a spatiotemporal manner. CircRNAs localized in the cytoplasm regulate mRNA translation or stability by binding to microRNAs and RNA-binding proteins (RBPs), while circRNAs in the nucleus regulate transcription and pre-mRNA splicing by associating with transcription factors and splicing factors. In this study, we sought to explore the interaction between circRNAs and chromatin. Analyzing published RNA-seq data from chromatin fractions identified hundreds of chromatin-associated circRNAs (cacRNAs) in various human cells. We validated the enrichment of a subset of circRNAs in the chromatin fraction and established the direct interaction of circDYNC1H1 and circKIF2C with chromatin in HEK293T cells. Furthermore, cacRNAs were found to interact with RBPs. Together, our research demonstrates the global association of hundreds of circRNAs with chromatin and expands our understanding of novel functional aspects of the circRNAs. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=186 SRC="FIGDIR/small/739476v1_ufig1.gif" ALT="Figure 1"> View larger version (69K): org.highwire.dtl.DTLVardef@804151org.highwire.dtl.DTLVardef@405206org.highwire.dtl.DTLVardef@c9373borg.highwire.dtl.DTLVardef@4903ea_HPS_FORMAT_FIGEXP M_FIG O_FLOATNOGraphical abstractC_FLOATNO C_FIG

molecular biology↗

bioRxiv2026

Vesicular pseudopodia define the fusion site on large secretory vesicles of the Drosophila salivary glands

Large secretory vesicles (LSVs) pose a scaling problem for regulated exocytosis. Their micron-scale dimensions greatly increase the vesicular membrane surface area, making productive engagement between the vesicular and target membrane fusion machinery unlikely. Here, we show that vesicular pseudopodia define the fusion sites of LSVs in Drosophila larval salivary glands. Focused ion beam scanning electron microscopy revealed that most LSVs project polarized pseudopodia that interconnect neighboring vesicles and orient toward the apical membrane. Exposed pseudopodia were frequently observed at the apical surface and associated with narrow fusion pores, indicating that fusion occurs at these structures. Three-dimensional correlative light and electron microscopy showed that the I-BAR protein Missing in Metastasis (MIM) selectively localizes to exposed pseudopodia. Proteomic analysis based on a MIM pull-down assay identified exocyst components, including Sec15, which localizes to pseudopodia and persists at fusion sites throughout secretion. Finally, the tetraspanin Tsp42Ee marked complementary apical fusion domains and was required for efficient exocytosis. Our findings support a model in which prepatterned vesicular and apical membrane domains coordinate efficient exocytosis. SummaryRegulated exocytosis of large secretory vesicles is facilitated by vesicular pseudopodia and an apical fusion domain that spatially organizes membrane tethering and fusion during secretion.

cell biology↗

bioRxiv2026

Connecting multiway enhancer-promoter interactions to changes in gene expression in cancer

Hi-C, and more recently Micro-C, experiments suggest that genome organization is altered as normal cells become cancerous, often resulting in aberrant gene expression. In prostate cancer, there is evidence that large topologically associating domains in normal cells split and are accompanied by shifts in the epigenetic marks from inactive to active states. However, it is unclear whether changes in genome organization alone can account for the gene expression increase in cancer cells. By combining polymer physics concepts and data-driven modeling, we first calculated an ensemble of three-dimensional (3D) chromatin structures using only the 2D contact map as input. The enhancer-promoter (E-P) distance distributions for the overexpressed Androgen Receptor (AR) and Forkhead Box Protein A1 (FOXA1) are broad, with mean values exceeding the threshold for direct E-P contact. Importantly, the average E-P distances decrease in the cancer cells, compared to normal cells in the AR locus, whereas in FOXA1 they are roughly constant or increase modestly. Similarly, the number of multiway contacts increases as cancer progresses across cancer cell lines in the AR locus. In contrast, the number of multiway contacts in FOXA1 is similar in normal and cancer cells. Because the 3D characteristics do not explain the enhanced gene expression in cancer cells, we developed Activity-by-Multiway-Contact (AMC) Model that integrates the multiway contacts with enhancer biochemical activity. The AMC model provides a plausible mechanism for the overexpression of both AR and FOXA1 in prostate cancer. Moreover, using Micro-C data for breast cancer, we show that the number of multiway enhancer-promoter contacts increases in four of five genes studied. When multiway contacts are combined with biochemical activity, changes in gene expression found in the experiment, positively correlate with the AMC score. The predictions of the AMC model not only account for overexpression of genes in prostate and breast cancer but also provide a basis for understanding gene expression variations in other genes as well.

genomics↗

bioRxiv2026

Punctuated Evolution of Endomembrane Compartments in Proto-Eukaryotes

Eukaryotic cells are defined by their endomembranes: compartments such as the endoplasmic reticulum (ER), Golgi and endosomes, exchanging cargo via vesicles. The evolutionary origins of endomembrane compartments remain unclear. Here we construct molecular-evolutionary trajectories for the stepwise addition of compartments after the emergence of the proto-ER in an ancestral eukaryote. We represent compartments and vesicles as nodes and edges of a directed graph. Vesicle budding and fusion regulators such as coats and SNAREs control cargo flows and determine compartment compositions. We computationally sample billions of possible graphs, and enumerate how duplication, deletion and mutation of regulators drive graph transitions. We find that evolutionary trajectories display punctuated shifts in compartment composition and number, interspersed with thousands of neutral mutations. The first added compartment inherits functions from the proto-ER or plasma membrane, or gains novel functions. Our results show how, given a billion years, simple molecular steps can generate complex endomembrane systems. SO_SCPLOWIGNIFICANCEC_SCPLOW SO_SCPLOWTATEMENTC_SCPLOWEukaryotic cells contain a system of endomembrane compartments that sort, process and deliver molecules to precise cellular destinations. This endomembrane system is a defining feature of all complex life, yet its evolutionary origins remain obscure. How did a proto-eukaryote with a single ancestral endomembrane compartment evolve into a cell with a Golgi, endosomes, lysosomes and other compartments characteristic of modern eukaryotes? We model this process from first principles, connecting the duplication, deletion and mutation of molecular regulators to compartment gain or loss. We find a punctuated pattern of endomembrane elaboration: a long phase of neutral exploration, driven by the mutation of duplicate gene copies, precedes the emergence of new compartments and functions.

evolutionary biology↗

bioRxiv2025

METTL3-mediated m6A modification of DNMT1 enhances ovarian cancer progression

High-grade serous carcinoma (HGSC), the most lethal subtype of ovarian cancer, is often diagnosed at advanced stages owing to its asymptomatic progression and lack of early detection markers. In this study, we identified a critical oncogenic role of the RNA methyltransferase METTL3 and the N6-methyladenosine (m6A) RNA modification pathway in HGSC. Depletion of METTL3 or its binding partner METTL14 impairs ovarian cancer proliferation and tumor progression. Mechanistically, m6A deposition enhances the translation of DNA methyltransferase DNMT1, an epigenetic repressor that silences tumor suppressor genes. Pharmacologic inhibition of DNMT1 led to DNA hypomethylation and upregulation of the tumor suppressors TNFAIP3 and FBXO32. Consistently, METTL3 depletion also increased the expression of these genes supporting a model in which METTL3 sustains oncogenesis by maintaining DNMT1 protein levels and repressing anti-tumor pathways. These findings position METTL3-mediated RNA modifications and DNMT1 as promising therapeutic targets in HGSC.

cancer biology↗

bioRxiv2025

Predicting statistics of gene translocation events: role of chromatin compaction and double-strand DNA break

How the 3D organization of chromatin affects gene translocation is an open question. By Monte Carlo simulation of translocation events in folded chromatin, we examine how the probability of translocation (Tij) is influenced by chromatin compaction and the occurrence of double-stranded DNA breaks (DSBs). Our results show that, beyond the two-segment contact probability, Tij depends on the overall compaction of the polymer and has a non-trivial contribution from multi-bead contacts and the probability of DSBs. We propose an empirical formula and provide analytical arguments for simple cases.

biophysics↗

bioRxiv2025

Fibrillarin shapes oncogenic protein pools and ribosomal composition in triple-negative breast cancer

Fibrillarin (FBL), a core component of the C/D box snoRNP complex, catalyzes 2-O-methylation (Nm) of ribosomal RNA (rRNA), influencing ribosome heterogeneity and oncogene translation. In triple-negative breast cancer (TNBC), FBL dysregulation creates an aberrant Nm signature. This study explores role of FBL in TNBC progression via translation-driven mechanisms. FBL knockdown impaired tumorigenic traits, induced metabolic stress, and reduced the translation efficiency of oncogenes, including metastasis-associated protein 1 (MTA1), interleukin-1 receptor-associated kinase 1 (IRAK1), and thymosin beta 10 (TMSB10). RiboMethSeq analysis revealed differential rRNA Nm site sensitivity to FBL depletion. Additionally, FBL knockdown lowered RPS28 protein levels, suggesting its misincorporation into ribosomes. Notably, silencing RPS28 also suppressed oncogenic traits and downregulated MTA1, IRAK1, and TMSB10, highlighting its role in FBL-mediated translation. These findings uncover a complex interplay between FBL, rRNA Nm modifications, and RPS28 in shaping oncogenic protein pools and ribosomal composition in TNBC. Targeting this pathway could offer novel therapeutic strategies for this aggressive cancer subtype.

molecular biology↗

bioRxiv2024

GET3B interacts with the thylakoidal ALB3 and ALB4 insertases and is involved in the initial stages of chloroplast biogenesis

Protein targeting and insertion into membranes are essential for cellular organization and organelle function. The Guided Entry of Tail-anchored (GET) pathway facilitates the post-translational targeting and insertion of tail-anchored (TA) membrane proteins. Arabidopsis thaliana has four GET3 homologues, including AtGET3B and AtGET3D localized to chloroplasts. These photosynthetic organelles possess complex membrane systems, and the mechanisms underlying their protein targeting and membrane biogenesis are not fully understood. This study conducted a comprehensive proteomic analysis of get3b mutant plastids, which displayed significant alterations. Fluorometric based complex assembly as well as CO2 assimilation analyses confirmed that disruption of GET3B function displayed a significant impact on photosystem II assembly as well as carbon fixation, respectively, indicating a functional role in chloroplast biogenesis. Additionally, genetic interactions were found between GET3B and the two component STIC system, which cooperates with the cpSRP pathway and is involved in the co-translational sorting of thylakoid proteins. Further, physical interactions were observed between GET3B and the C-terminus of ALB3 and ALB4 in vitro and the full length proteins in vivo, indicating a role of GET3B in protein targeting and membrane integration within chloroplasts. These findings enhance our understanding of GET3Bs involvement in stromal protein targeting and thylakoidal biogenesis.

cell biology↗

bioRxiv2024

Genome-wide Identification of the Laccase Gene Family in White Jute (Corchorus capsularis): Potential Targets for Lignin Engineering in Bast Fiber

Jute (Corchorus spp.) is an important industrial bast fibre crop valued for its lignocellulosic fibres, yet the molecular basis of fibre lignification remains unexplored. Laccase (EC 1.10.3.2) is a key enzyme catalysing the final steps of lignin polymerisation. A genome-wide analysis of white jute (Corchorus capsularis) identified 32 putative laccase genes (CcaLACs) that were phylogenetically grouped into six clades. Expression profiling revealed predominant expression in phloem tissue (16 genes), followed by leaf (8) and xylem/root tissues (4). Several CcaLACs showed progressive upregulation from early growth to harvest stages. Homology with Arabidopsis laccases highlighted candidate genes involved in lignification, which were further supported by transcriptomic and qRT-PCR analyses. Notably, key CcaLACs showed significantly reduced expression in dlpf (deficient lignified phloem fibre), a low-lignin white jute mutant. CcaLAC expression was also responsive to abiotic stresses, including abscisic acid and copper. MicroRNA target prediction identified Ath-miR397a and Ath-miR397b as potential regulators of multiple CcaLACs. Structural and subcellular analyses revealed conserved motifs, transmembrane domains, and diverse cellular localisation. Gene ontology analysis linked CcaLACs to lignin and phenylpropanoid biosynthesis. Among them, CcaLAC28 and CcaLAC32 emerged as strong candidate genes associated with phloem fibre lignification, representing promising targets for future functional validation towards developing low-lignin jute varieties.

plant biology↗

bioRxiv2024

Targeting transcription factors through an IMiD independent zinc finger domain

Immunomodulatory imide drugs (IMiDs) degrade specific C2H2 zinc finger degrons in transcription factors, making them effective against certain cancers. SALL4, a cancer driver, contains seven C2H2 zinc fingers in four clusters, including an IMiD degron in zinc finger cluster two (ZFC2). Surprisingly, IMiDs do not inhibit growth of SALL4 expressing cancer cells. To overcome this limit, we focused on a non-IMiD degron, SALL4 zinc finger cluster four (ZFC4). By combining AlphaFold and the ZFC4-DNA crystal structure, we identified a potential ZFC4 drug pocket. Utilizing an in silico docking algorithm and cell viability assays, we screened chemical libraries and discovered SH6, which selectively targets SALL4-expressing cancer cells. Mechanistic studies revealed that SH6 degrades SALL4 protein through the CUL4A/CRBN pathway, while deletion of ZFC4 abolished this activity. Moreover, SH6 led to significant 62% tumor growth inhibition of SALL4+ xenografts in vivo and demonstrated good bioavailability in pharmacokinetic studies. In summary, these studies represent a new approach for IMiD independent drug discovery targeting C2H2 transcription factors in cancer. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=177 SRC="FIGDIR/small/574032v1_ufig1.gif" ALT="Figure 1"> View larger version (27K): org.highwire.dtl.DTLVardef@b8e4e8org.highwire.dtl.DTLVardef@bc6f01org.highwire.dtl.DTLVardef@11bbe85org.highwire.dtl.DTLVardef@791cb1_HPS_FORMAT_FIGEXP M_FIG C_FIG

cancer biology↗

bioRxiv2023

SALL4B, not targeted by IMiD, is important for SALL4-mediated tumorigenesis

Immunomodulatory (IMiD) drugs have shown a prominent therapeutic activity in hematologic malignancies; however, their usage in solid tumors is limited. The oncofetal protein SALL4 is essential for cancer cell survival. While IMiDs can induce SALL4 degradation, they fail to induce cell death in SALL4-expressing cancer cell lines. Here, we observed that this inefficacy arose from their selective degradation of the long SALL4 isoform, while sparing the short SALL4B isoform. Selective silencing of SALL4B phenocopied total SALL4 depletion by inducing cancer apoptosis, underscoring the critical role of SALL4B in cancer maintenance. Recognizing that IMiDs cant degrade SALL4B, we performed a high-throughput screen to identify compound(s) that could achieve this. We identified a small molecule compound that degrades both SALL4 isoforms with enhanced potency towards SALL4B in a cereblon- and proteasome-dependent manner. This compound suppressed cancer cell proliferation and attenuated tumor development in both cell line and patient-derived xenograft models. Transcriptomic analyses further revealed convergent effects of genetic and pharmacologic SALL4B depletion on DNA damage response and replication pathways. Together, these findings identify SALL4B as the therapeutically relevant isoform in SALL4-dependent cancers and establish isoform-aware targeted degradation as a strategy to overcome the limitation of IMiDs in solid tumors. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=142 SRC="FIGDIR/small/548071v2_ufig1.gif" ALT="Figure 1"> View larger version (66K): org.highwire.dtl.DTLVardef@99670dorg.highwire.dtl.DTLVardef@13ca58forg.highwire.dtl.DTLVardef@998e7eorg.highwire.dtl.DTLVardef@15a1875_HPS_FORMAT_FIGEXP M_FIG Graphical Abstract | Identification of QE: a non-IMiDs degrader capable of degrading both SALL4A and SALL4B, triggers anti-cancer effects beyond IMiDs, and Impacts of QE on Key Validated SALL4B Targets and Pathways C_FIG

cancer biology↗

bioRxiv2023

The catalytic-independent function of LSD1 modulates the epigenetic landscape of mouse embryonic stem cells

Lysine-specific histone demethylase 1 (LSD1), which demethylates mono- or di-methylated histone H3 on lysine 4 (H3K4me1/2), is essential for early embryogenesis and development. Here we show that LSD1 is dispensable for embryonic stem cell (ESC) self-renewal but is required for ESC growth and differentiation. Reexpression of a catalytically-dead LSD1 (LSD1MUT) recovers the proliferation capability of ESCs, yet the enzymatic activity of LSD1 is essential to ensure proper differentiation. Indeed, a gain of H3K4me1 in Lsd1 knockout (KO) ESCs does not lead to major changes in global gene expression programs related to stemness. However, ablation of LSD1 but not LSD1MUT results in decreased DNMT1 and UHRF1 proteins coupled to global hypomethylation. We show that both LSD1 and LSD1MUT control protein stability of UHRF1 and DNMT1 through interaction with the ubiquitin-specific peptidase 7 (USP7) and, consequently, inhibiting DNMT1 and UHRF1 ubiquitylation. Our studies elucidate for the first time a novel mechanism by which the scaffolding function of LSD1 controls DNA methylation in ESCs.

molecular biology↗

bioRxiv2022

Violation of rationality in shoaling decision making in zebrafish (Danio rerio)

The decoy effect, a bias in choice between two options when a third, inferior option is introduced, has been observed across various organisms, from slime molds to humans. In this study, we investigated whether zebrafish (Danio rerio), a widely used biological model organism, exhibit the decoy effect in their shoaling group choices, specifically examining this effect by varying only shoal size. Using spatial trajectory analysis of freely swimming zebrafish interacting with conspecifics in adjacent display tanks, we tested how shoaling decisions varied between dichotomous (two-option) and trichotomous (three-option) choice sets. Our experiments compared preferences for 4 versus 2 and 6 versus 3 shoal sizes, with a single fish serving as a decoy in the trichotomous sets. The results revealed sex-specific differences in the decoy effect: males exhibited a shift in preference only in the Trichotomous-first condition, where prior exposure to the decoy led to a significant preference for the larger shoal. In contrast, females displayed the decoy effect exclusively in the Dichotomous-first condition, shifting from a significant preference for the larger shoal to showing no clear preference in the presence of the decoy. Notably, our findings demonstrate that the decoy effect can occur even when studied unidimensionally, with both sex and the order of presentation influencing zebrafish shoaling preferences. These results offer new insights into decision-making processes and highlight the importance of considering order effects in studies of choice behavior, with potential methodological implications for research in other species.

animal behavior and cognition↗

bioRxiv2022

Predicting scale-dependent chromatin polymer properties from systematic coarse-graining

Simulating chromatin is crucial for predicting genome organization and dynamics. Even though coarse-grained bead-spring polymer models are commonly used to describe chromatin, the relevant bead dimensions, elastic properties, and the nature of inter-bead potentials are unknown. Using publicly available nucleosome-resolution contact probability (Micro-C) data, we systematically coarse-grain chromatin and predict quantities essential for polymer representation of chromatin. We compute size distributions of chromatin beads for different coarse-graining scales, quantify fluctuations and distributions of bond lengths between neighboring regions, and derive effective spring constant values. Unlike the prevalent notion, our findings argue that coarse-grained chromatin beads must be considered as soft particles that can overlap, and we derive an effective inter-bead soft potential and quantify an overlap parameter. We also compute angle distributions between neighboring bonds giving insights into intrinsic folding and local bendability of chromatin. While the nucleosome-linker DNA bond angle naturally emerges from our work, we show that there are two populations of local structural states. The bead sizes, bond lengths, and bond angles show different mean behavior at Topologically Associating Domain (TAD) boundaries and TAD interiors. We integrate our findings into a coarse-grained polymer model and provide quantitative estimates of all model parameters, which can serve as a foundational basis for all future coarse-grained chromatin simulations.

biophysics↗

bioRxiv2021

Spatiotemporal organization of chromatin domains: role of interaction energy and polymer entropy

Chromatin is known to be organized into multiple domains of varying sizes and compaction. While these domains are often imagined as static structures, they are highly dynamic and show cell-to-cell variability. Since processes such as gene regulation and DNA replication occur in the context of these domains, it is important to understand their organization, fluctuation and dynamics. To simulate chromatin domains, one requires knowledge of interaction strengths among chromatin segments. Here, we derive interaction strength parameters from experimentally known contact maps and use them to predict chromatin organization and dynamics. Taking two domains on the human chromosome as examples, we investigate its 3D organization, size/shape fluctuations, and dynamics of different segments within a domain, accounting for hydrodynamic effects. Considering different cell types, we quantify changes in interaction strengths and chromatin shape fluctuations in different epigenetic states. Perturbing the interaction strengths systematically, we further investigate how epigenetic-like changes can alter the spatio-temporal nature of the domains. Our results show that heterogeneous weak interactions are crucial in determining the organization of the domains. Computing effective stiffness and relaxation times, we investigate how perturbations in interactions affect the solid-like and liquid-like nature of chromatin domains. Quantifying dynamics of chromatin segments within a domain, we show how the competition between polymer entropy and interaction energy influence the timescales of loop formation and maintenance of stable loops.

biophysics↗

bioRxiv2021

Female gametophyte expressed Arabidopsis thaliana lipid transfer proteins AtLtpI.4 and AtLtpI.8 provide a link between callose homeostasis, pollen tube guidance, and fertilization success

Non-specific lipid transfer proteins (LTPs) represent a sub-class among the large family of Cysteine-rich proteins (CRPs) specific to land plants. LTPs possess a hydrophobic cavity, enabling them to bind and stabilize a variety of lipid molecules outside membranes. In line with the existence of an N-terminal signal peptide, secreted LTPs represent a well-suited mobile signal carrier in the plants extracellular matrix. Thus, LTPs are currently considered as key players to mediate the bulk flow of lipids between membranes/compartments as well as the buildup of lipid barrier polymers including cutin and suberin. Here, we show that floral expressed Arabidopsis thaliana AtLtpI.4 (AtLTP2) and AtLtpI.8 (AtLTP5), mutually control cell-cell communication between growing pollen tubes and ovules during fertilization. Arabidopsis mutants lacking functional AtLtpI.4 and AtLtpI.8 exhibit significantly reduced fertilization success. Cross-pollination and cell biological analyses revealed that AtLtpI.4/I.8 double mutants are impaired in pollen tube guidance towards ovules. Our finding that the AtLtpI.4/I.8 phenotype correlates with aberrant callose depositions in the micropylar region during ovule development suggests that both LTPs represent novel players of a joint signaling pathway that controls callose homeostasis in the female gametophyte.

plant biology↗