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Article ; Online: Transcriptional bodies manage tight resources.

Stec, Natalia / Klosin, Adam

2024 Volume 26, Issue 4, Page(s) 512–513

MeSH term(s)	Transcription, Genetic ; Epithelial Cells
Language	English
Publishing date	2024-04-06
Publishing country	England
Document type	Journal Article
ZDB-ID	1474722-4
ISSN	1476-4679 ; 1465-7392
ISSN (online)	1476-4679
ISSN	1465-7392
DOI	10.1038/s41556-024-01395-x
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Zs.A 5169: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article: The Full-Size ABCG Transporter of

Banasiak, Joanna / Borghi, Lorenzo / Stec, Natalia / Martinoia, Enrico / Jasiński, Michał

Frontiers in plant science

2020 Volume 11, Page(s) 18

Abstract: Strigolactones (SLs) are plant-derived signaling molecules that stimulate the hyphal branching of arbuscular mycorrhizal fungi (AMF), and consequently promote symbiotic interaction between the fungus and the plant. Currently, our knowledge on the ... ...

Abstract	Strigolactones (SLs) are plant-derived signaling molecules that stimulate the hyphal branching of arbuscular mycorrhizal fungi (AMF), and consequently promote symbiotic interaction between the fungus and the plant. Currently, our knowledge on the molecular mechanism of SL transport is restricted to the
Language	English
Publishing date	2020-02-07
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2613694-6
ISSN	1664-462X
ISSN	1664-462X
DOI	10.3389/fpls.2020.00018
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Article ; Online: A circadian-like gene network programs the timing and dosage of heterochronic miRNA transcription during C. elegans development.

Kinney, Brian / Sahu, Shubham / Stec, Natalia / Hills-Muckey, Kelly / Adams, Dexter W / Wang, Jing / Jaremko, Matt / Joshua-Tor, Leemor / Keil, Wolfgang / Hammell, Christopher M

Developmental cell

2023 Volume 58, Issue 22, Page(s) 2563–2579.e8

Abstract: Development relies on the exquisite control of both the timing and the levels of gene expression to achieve robust developmental transitions. How cis- and trans-acting factors control both aspects simultaneously is unclear. We show that transcriptional ... ...

Abstract	Development relies on the exquisite control of both the timing and the levels of gene expression to achieve robust developmental transitions. How cis- and trans-acting factors control both aspects simultaneously is unclear. We show that transcriptional pulses of the temporal patterning microRNA (miRNA) lin-4 are generated by two nuclear hormone receptors (NHRs) in C. elegans, NHR-85 and NHR-23, whose mammalian orthologs, Rev-Erb and ROR, function in the circadian clock. Although Rev-Erb and ROR antagonize each other to control once-daily transcription in mammals, NHR-85/NHR-23 heterodimers bind cooperatively to lin-4 regulatory elements to induce a single pulse of expression during each larval stage. Each pulse's timing, amplitude, and duration are dictated by the phased expression of these NHRs and the C. elegans Period ortholog, LIN-42, that binds to and represses NHR-85. Therefore, during nematode temporal patterning, an evolutionary rewiring of circadian clock components couples the timing of gene expression to the control of transcriptional dosage.
MeSH term(s)	Animals ; Caenorhabditis elegans/metabolism ; Caenorhabditis elegans Proteins/genetics ; Caenorhabditis elegans Proteins/metabolism ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Gene Regulatory Networks ; Gene Expression Regulation, Developmental ; Receptors, Cytoplasmic and Nuclear/metabolism ; Mammals/metabolism ; Transcription Factors/genetics ; Transcription Factors/metabolism
Chemical Substances	Caenorhabditis elegans Proteins ; MicroRNAs ; Receptors, Cytoplasmic and Nuclear ; LIN-42 protein, C elegans ; Transcription Factors
Language	English
Publishing date	2023-08-28
Publishing country	United States
Document type	Journal Article
ZDB-ID	2054967-2
ISSN	1878-1551 ; 1534-5807
ISSN (online)	1878-1551
ISSN	1534-5807
DOI	10.1016/j.devcel.2023.08.006
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Zs.A 5742: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 76: Show issues

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Article ; Online: Abscisic acid - an overlooked player in plant-microbe symbioses formation?

Stec, Natalia / Banasiak, Joanna / Jasiński, Michał

Acta biochimica Polonica

2016 Volume 63, Issue 1, Page(s) 53–58

Abstract: Abscisic acid (ABA) is an ubiquitous plant hormone and one of the foremost signalling molecules, controlling plants' growth and development, as well as their response to environmental stresses. To date, the function of ABA has been extensively ... ...

Abstract	Abscisic acid (ABA) is an ubiquitous plant hormone and one of the foremost signalling molecules, controlling plants' growth and development, as well as their response to environmental stresses. To date, the function of ABA has been extensively investigated as an abiotic stress molecule which regulates the plants' water status. However, in the context of symbiotic associations, ABA is less recognized. In contrast to well-described auxin/cytokinin and gibberellin/strigolactone involvement in symbioses, ABA has long been underestimated. Interestingly, ABA emerges as an important player in arbuscular mycorrhiza and legume-rhizobium symbiosis. The plant's use of stress hormones like ABA in regulation of those interactions directly links the efficiency of these processes to the environmental status of the plant, notably during drought stress. Here we provide an overview of ABA interplay in beneficial associations of plants with microorganisms and propose ABA as a potential factor determining whether the investment in establishing the interaction is higher than the profit coming from it.
MeSH term(s)	Abscisic Acid/metabolism ; Mycorrhizae/physiology ; Plants/microbiology ; Rhizobium/physiology ; Symbiosis
Chemical Substances	Abscisic Acid (72S9A8J5GW)
Language	English
Publishing date	2016-02-01
Publishing country	Poland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	595762-x
ISSN	1734-154X ; 0001-527X
ISSN (online)	1734-154X
ISSN	0001-527X
DOI	10.18388/abp.2015_1210
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Article ; Online: An Epigenetic Priming Mechanism Mediated by Nutrient Sensing Regulates Transcriptional Output during C. elegans Development.

Stec, Natalia / Doerfel, Katja / Hills-Muckey, Kelly / Ettorre, Victoria M / Ercan, Sevinc / Keil, Wolfgang / Hammell, Christopher M

Current biology : CB

2020 Volume 31, Issue 4, Page(s) 809–826.e6

Abstract: Although precise tuning of gene expression levels is critical for most developmental pathways, the mechanisms by which the transcriptional output of dosage-sensitive molecules is established or modulated by the environment remain poorly understood. Here, ...

Abstract	Although precise tuning of gene expression levels is critical for most developmental pathways, the mechanisms by which the transcriptional output of dosage-sensitive molecules is established or modulated by the environment remain poorly understood. Here, we provide a mechanistic framework for how the conserved transcription factor BLMP-1/Blimp1 operates as a pioneer factor to decompact chromatin near its target loci during embryogenesis (hours prior to major transcriptional activation) and, by doing so, regulates both the duration and amplitude of subsequent target gene transcription during post-embryonic development. This priming mechanism is genetically separable from the mechanisms that establish the timing of transcriptional induction and functions to canalize aspects of cell-fate specification, animal size regulation, and molting. A key feature of the BLMP-1-dependent transcriptional priming mechanism is that chromatin decompaction is initially established during embryogenesis and maintained throughout larval development by nutrient sensing. This anticipatory mechanism integrates transcriptional output with environmental conditions and is essential for resuming normal temporal patterning after animals exit nutrient-mediated developmental arrests.
MeSH term(s)	Animals ; Caenorhabditis elegans/genetics ; Caenorhabditis elegans/metabolism ; Caenorhabditis elegans Proteins/genetics ; Caenorhabditis elegans Proteins/metabolism ; Chromatin ; Epigenesis, Genetic ; Gene Expression Regulation, Developmental ; Nutrients ; Transcription Factors/metabolism
Chemical Substances	Caenorhabditis elegans Proteins ; Chromatin ; Transcription Factors
Language	English
Publishing date	2020-12-22
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1071731-6
ISSN	1879-0445 ; 0960-9822
ISSN (online)	1879-0445
ISSN	0960-9822
DOI	10.1016/j.cub.2020.11.060
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Article ; Online: Sentryn and SAD Kinase Link the Guided Transport and Capture of Dense Core Vesicles in

Morrison, Logan M / Edwards, Stacey L / Manning, Laura / Stec, Natalia / Richmond, Janet E / Miller, Kenneth G

Genetics

2018 Volume 210, Issue 3, Page(s) 925–946

Abstract: Dense core vesicles (DCVs) can transmit signals by releasing neuropeptides from specialized synaptic regions called active zones. DCVs reach the active zone by motorized transport through a long axon. A reverse motor frequently interrupts progress by ... ...

Abstract	Dense core vesicles (DCVs) can transmit signals by releasing neuropeptides from specialized synaptic regions called active zones. DCVs reach the active zone by motorized transport through a long axon. A reverse motor frequently interrupts progress by taking DCVs in the opposite direction. "Guided transport" refers to the mechanism by which outward movements ultimately dominate to bring DCVs to the synaptic region. After guided transport, DCVs alter their interactions with motors and enter a "captured" state. The mechanisms of guided transport and capture of DCVs are unknown. Here, we discovered two proteins that contribute to both processes in
MeSH term(s)	Animals ; Axons/metabolism ; Biological Transport ; Caenorhabditis elegans/cytology ; Caenorhabditis elegans/enzymology ; Caenorhabditis elegans/genetics ; Caenorhabditis elegans/metabolism ; Caenorhabditis elegans Proteins/metabolism ; Dyneins/metabolism ; Mutation ; Nerve Tissue Proteins/metabolism ; Protein Serine-Threonine Kinases/metabolism ; Secretory Vesicles/metabolism
Chemical Substances	Caenorhabditis elegans Proteins ; Nerve Tissue Proteins ; Sentryn protein, C elegans ; Protein Serine-Threonine Kinases (EC 2.7.11.1) ; Dyneins (EC 3.6.4.2)
Language	English
Publishing date	2018-11-06
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2167-2
ISSN	1943-2631 ; 0016-6731
ISSN (online)	1943-2631
ISSN	0016-6731
DOI	10.1534/genetics.118.300847
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Article ; Online: Sentryn Acts with a Subset of Active Zone Proteins To Optimize the Localization of Synaptic Vesicles in

Edwards, Stacey L / Morrison, Logan M / Manning, Laura / Stec, Natalia / Richmond, Janet E / Miller, Kenneth G

Genetics

2018 Volume 210, Issue 3, Page(s) 947–968

Abstract: Synaptic vesicles (SVs) transmit signals by releasing neurotransmitters from specialized synaptic regions of neurons. In the synaptic region, SVs are tightly clustered around small structures called active zones. The motor KIF1A transports SVs outward ... ...

Abstract	Synaptic vesicles (SVs) transmit signals by releasing neurotransmitters from specialized synaptic regions of neurons. In the synaptic region, SVs are tightly clustered around small structures called active zones. The motor KIF1A transports SVs outward through axons until they are captured in the synaptic region. This transport must be guided in the forward direction because it is opposed by the dynein motor, which causes SVs to reverse direction multiple times en route. The core synapse stability (CSS) system contributes to both guided transport and capture of SVs. We identified Sentryn as a CSS protein that contributes to the synaptic localization of SVs in
MeSH term(s)	Animals ; Axons/metabolism ; Caenorhabditis elegans/cytology ; Caenorhabditis elegans/genetics ; Caenorhabditis elegans/metabolism ; Caenorhabditis elegans Proteins/metabolism ; Dendrites/metabolism ; Dyneins/metabolism ; Lysosomes/metabolism ; Mutation ; Nerve Tissue Proteins/metabolism ; Protein Transport ; Synaptic Vesicles/metabolism
Chemical Substances	Caenorhabditis elegans Proteins ; Nerve Tissue Proteins ; Sentryn protein, C elegans ; Dyneins (EC 3.6.4.2)
Language	English
Publishing date	2018-11-06
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2167-2
ISSN	1943-2631 ; 0016-6731
ISSN (online)	1943-2631
ISSN	0016-6731
DOI	10.1534/genetics.118.301466
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Article ; Online: PQN-59 antagonizes microRNA-mediated repression during post-embryonic temporal patterning and modulates translation and stress granule formation in C. elegans.

Carlston, Colleen / Weinmann, Robin / Stec, Natalia / Abbatemarco, Simona / Schwager, Francoise / Wang, Jing / Ouyang, Huiwu / Ewald, Collin Y / Gotta, Monica / Hammell, Christopher M

PLoS genetics

2021 Volume 17, Issue 11, Page(s) e1009599

Abstract: microRNAs (miRNAs) are potent regulators of gene expression that function in a variety of developmental and physiological processes by dampening the expression of their target genes at a post-transcriptional level. In many gene regulatory networks (GRNs), ...

Abstract	microRNAs (miRNAs) are potent regulators of gene expression that function in a variety of developmental and physiological processes by dampening the expression of their target genes at a post-transcriptional level. In many gene regulatory networks (GRNs), miRNAs function in a switch-like manner whereby their expression and activity elicit a transition from one stable pattern of gene expression to a distinct, equally stable pattern required to define a nascent cell fate. While the importance of miRNAs that function in this capacity are clear, we have less of an understanding of the cellular factors and mechanisms that ensure the robustness of this form of regulatory bistability. In a screen to identify suppressors of temporal patterning phenotypes that result from ineffective miRNA-mediated target repression, we identified pqn-59, an ortholog of human UBAP2L, as a novel factor that antagonizes the activities of multiple heterochronic miRNAs. Specifically, we find that depletion of pqn-59 can restore normal development in animals with reduced lin-4 and let-7-family miRNA activity. Importantly, inactivation of pqn-59 is not sufficient to bypass the requirement of these regulatory RNAs within the heterochronic GRN. The pqn-59 gene encodes an abundant, cytoplasmically-localized, unstructured protein that harbors three essential "prion-like" domains. These domains exhibit LLPS properties in vitro and normally function to limit PQN-59 diffusion in the cytoplasm in vivo. Like human UBAP2L, PQN-59's localization becomes highly dynamic during stress conditions where it re-distributes to cytoplasmic stress granules and is important for their formation. Proteomic analysis of PQN-59 complexes from embryonic extracts indicates that PQN-59 and human UBAP2L interact with orthologous cellular components involved in RNA metabolism and promoting protein translation and that PQN-59 additionally interacts with proteins involved in transcription and intracellular transport. Finally, we demonstrate that pqn-59 depletion reduces protein translation and also results in the stabilization of several mature miRNAs (including those involved in temporal patterning). These data suggest that PQN-59 may ensure the bistability of some GRNs that require miRNA functions by promoting miRNA turnover and, like UBAP2L, enhancing protein translation.
MeSH term(s)	Animals ; Body Patterning/physiology ; Caenorhabditis elegans/genetics ; Caenorhabditis elegans/metabolism ; Caenorhabditis elegans Proteins/genetics ; Caenorhabditis elegans Proteins/physiology ; Carrier Proteins/metabolism ; Gene Deletion ; Gene Expression Regulation ; Intracellular Signaling Peptides and Proteins/genetics ; Intracellular Signaling Peptides and Proteins/physiology ; MicroRNAs/physiology ; Protein Biosynthesis/physiology ; RNA Processing, Post-Transcriptional ; Stress Granules/metabolism
Chemical Substances	Caenorhabditis elegans Proteins ; Carrier Proteins ; Intracellular Signaling Peptides and Proteins ; MicroRNAs ; Ubap2L protein, human ; pqn-59 protein, C elegans
Language	English
Publishing date	2021-11-22
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2186725-2
ISSN	1553-7404 ; 1553-7390
ISSN (online)	1553-7404
ISSN	1553-7390
DOI	10.1371/journal.pgen.1009599
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Article ; Online: A

Aguirre-Chen, Cristina / Stec, Natalia / Ramos, Olivia Mendivil / Kim, Nuri / Kramer, Melissa / McCarthy, Shane / Gillis, Jesse / McCombie, W Richard / Hammell, Christopher M

G3 (Bethesda, Md.)

2020 Volume 10, Issue 5, Page(s) 1617–1628

Abstract: Analysis of patient-derived DNA samples has identified hundreds of variants that are likely involved in neuropsychiatric diseases such as autism spectrum disorder (ASD) and schizophrenia (SCZ). While these studies couple behavioral phenotypes to ... ...

Abstract	Analysis of patient-derived DNA samples has identified hundreds of variants that are likely involved in neuropsychiatric diseases such as autism spectrum disorder (ASD) and schizophrenia (SCZ). While these studies couple behavioral phenotypes to individual genotypes, the number and diversity of candidate genes implicated in these disorders highlights the fact that the mechanistic underpinnings of these disorders are largely unknown. Here, we describe a RNAi-based screening platform that uses
MeSH term(s)	Animals ; Autism Spectrum Disorder/genetics ; Caenorhabditis elegans/genetics ; Caenorhabditis elegans/metabolism ; Caenorhabditis elegans Proteins/genetics ; Caenorhabditis elegans Proteins/metabolism ; Humans ; RNA Interference ; Transcription Factors/genetics
Chemical Substances	Caenorhabditis elegans Proteins ; Transcription Factors
Language	English
Publishing date	2020-05-04
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2629978-1
ISSN	2160-1836 ; 2160-1836
ISSN (online)	2160-1836
ISSN	2160-1836
DOI	10.1534/g3.119.400925
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Article ; Online: An engineered, orthogonal auxin analog/AtTIR1(F79G) pairing improves both specificity and efficacy of the auxin degradation system in Caenorhabditis elegans.

Hills-Muckey, Kelly / Martinez, Michael A Q / Stec, Natalia / Hebbar, Shilpa / Saldanha, Joanne / Medwig-Kinney, Taylor N / Moore, Frances E Q / Ivanova, Maria / Morao, Ana / Ward, J D / Moss, Eric G / Ercan, Sevinc / Zinovyeva, Anna Y / Matus, David Q / Hammell, Christopher M

Genetics

2021 Volume 220, Issue 2

Abstract: The auxin-inducible degradation system in C. elegans allows for spatial and temporal control of protein degradation via heterologous expression of a single Arabidopsis thaliana F-box protein, transport inhibitor response 1 (AtTIR1). In this system, ... ...

Abstract	The auxin-inducible degradation system in C. elegans allows for spatial and temporal control of protein degradation via heterologous expression of a single Arabidopsis thaliana F-box protein, transport inhibitor response 1 (AtTIR1). In this system, exogenous auxin (Indole-3-acetic acid; IAA) enhances the ability of AtTIR1 to function as a substrate recognition component that adapts engineered degron-tagged proteins to the endogenous C. elegans E3 ubiquitin ligases complex [SKR-1/2-CUL-1-F-box (SCF)], targeting them for degradation by the proteosome. While this system has been employed to dissect the developmental functions of many C. elegans proteins, we have found that several auxin-inducible degron (AID)-tagged proteins are constitutively degraded by AtTIR1 in the absence of auxin, leading to undesired loss-of-function phenotypes. In this manuscript, we adapt an orthogonal auxin derivative/mutant AtTIR1 pair [C. elegans AID version 2 (C.e.AIDv2)] that transforms the specificity of allosteric regulation of TIR1 from IAA to one that is dependent on an auxin derivative harboring a bulky aryl group (5-Ph-IAA). We find that a mutant AtTIR1(F79G) allele that alters the ligand-binding interface of TIR1 dramatically reduces ligand-independent degradation of multiple AID-tagged proteins. In addition to solving the ectopic degradation problem for some AID-targets, the addition of 5-Ph-IAA to culture media of animals expressing AtTIR1(F79G) leads to more penetrant loss-of-function phenotypes for AID-tagged proteins than those elicited by the AtTIR1-IAA pairing at similar auxin analog concentrations. The improved specificity and efficacy afforded by the mutant AtTIR1(F79G) allele expand the utility of the AID system and broaden the number of proteins that can be effectively targeted with it.
MeSH term(s)	Animals ; Arabidopsis/genetics ; Arabidopsis/metabolism ; Arabidopsis Proteins/genetics ; Caenorhabditis elegans/genetics ; Caenorhabditis elegans/metabolism ; Caenorhabditis elegans Proteins/genetics ; Caenorhabditis elegans Proteins/metabolism ; F-Box Proteins/genetics ; F-Box Proteins/metabolism ; Indoleacetic Acids/metabolism
Chemical Substances	Arabidopsis Proteins ; Caenorhabditis elegans Proteins ; F-Box Proteins ; Indoleacetic Acids
Language	English
Publishing date	2021-08-14
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2167-2
ISSN	1943-2631 ; 0016-6731
ISSN (online)	1943-2631
ISSN	0016-6731
DOI	10.1093/genetics/iyab174
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