A NanoDam toolkit for tissue-specific transcription factor profiling in<i>C. elegans</i>

Yee, Callista; Xiao, Yutong; Katsanos, Dimitris; Medwig-Kinney, Taylor N.; Zhang, Wan; Shen, Kang; Matus, David Q.; Barkoulas, Michalis

doi:10.1101/2023.05.31.543105

Cited by 4 publications

(1 citation statement)

References 45 publications

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“…To identify downstream targets of EFL-3 in the seam cells, we used a modified TaDa approach for streamlined tissue-specific transcription factor binding called NanoDam 60, 61 . NanoDam employs the main TaDa principle to overcome the considerable toxicity observed when Dam-fusions are expressed at high levels in animal cells 35, 62 .…”

Section: Resultsmentioning

confidence: 99%

EFL-3/E2F7 modulates Wnt signalling through repressing the LIT-1 Nemo-like kinase during asymmetric epidermal cell division inCaenorhabditis elegans

Ferrando-Marco,

Barkoulas

2024

Preprint

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The E2F family of transcription factors is conserved in higher eukaryotes and plays pivotal roles in controlling gene expression during the cell cycle. Most canonical E2Fs associate with members of the Dimerisation Partner (DP) family to activate or repress target genes. However, atypical repressors, such as E2F7 and E2F8, lack DP interaction domains and their functions are less understood. We report here that EFL-3, the E2F7 homologue ofC. elegans, regulates epidermal stem cell differentiation. We show that phenotypic defects inefl-3mutants depend on the Nemo-like kinaselit-1.EFL-3 represseslit-1expression through direct binding to alit-1intronic element. Increased LIT-1 expression inefl-3mutants reduces POP-1/TCF nuclear distribution, and consequently alters Wnt pathway activation. Our findings provide a mechanistic link between an atypical E2F family member and NLK duringC. elegansasymmetric cell division, which may be conserved in other animals.HighlightsEFL-3 is enriched in anterior daughter cells following asymmetric seam cell division.efl-3mutants show defects in cell differentiation and seam cell fate maintenance.EFL-3 directly represseslit-1/NLK expression.EFL-3-mediatedlit-1repression alters POP-1 nuclear levels, linking EFL-3 to Wnt signalling.

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Section: Resultsmentioning

confidence: 99%

EFL-3/E2F7 modulates Wnt signalling through repressing the LIT-1 Nemo-like kinase during asymmetric epidermal cell division inCaenorhabditis elegans

Ferrando-Marco,

Barkoulas

2024

Preprint

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An activity-regulated transcriptional program directly drives synaptogenesis

Yee,

Xiao,

Chen

et al. 2024

Nat Neurosci

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Although the molecular composition and architecture of synapses have been widely explored, much less is known about what genetic programs directly activate synaptic gene expression and how they are modulated. Here, using Caenorhabditis elegans dopaminergic neurons, we reveal that EGL-43/MECOM and FOS-1/FOS control an activity-dependent synaptogenesis program. Loss of either factor severely reduces presynaptic protein expression. Both factors bind directly to promoters of synaptic genes and act together with CUT homeobox transcription factors to activate transcription. egl-43 and fos-1 mutually promote each other’s expression, and increasing the binding affinity of FOS-1 to the egl-43 locus results in increased presynaptic protein expression and synaptic function. EGL-43 regulates the expression of multiple transcription factors, including activity-regulated factors and developmental factors that define multiple aspects of dopaminergic identity. Together, we describe a robust genetic program underlying activity-regulated synapse formation during development.

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Cell cycle perturbation uncouples mitotic progression and invasive behavior in a post-mitotic cell

Martinez

Zhao

Moore

et al. 2023

Preprint

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The acquisition of the post-mitotic state is crucial for the execution of many terminally differentiated cell behaviors during organismal development. However, the mechanisms that maintain the post-mitotic state in this context remain poorly understood. To gain insight into these mechanisms, we used the genetically and visually accessible model of C. elegans anchor cell (AC) invasion into the vulval epithelium. The AC is a terminally differentiated uterine cell that must exit the cell cycle and enter a post-mitotic to initiate contact between the uterus and vulva through a cell invasion event. Here, we set out to identify the negative cell cycle regulators that maintain the AC in a post-mitotic, invasive state. Although our findings revealed a critical role for CKI-1 (p21CIP1/p27KIP1) in maintaining the post-mitotic state of the AC, loss of CKI-1 alone or in combination with other negative cell cycle regulators-including CKI-2 (p21CIP1/p27KIP1), LIN-35 (pRb/p107/p130), FZR-1 (Cdh1/Hct1), and LIN-23 (Beta-TrCP) resulted in proliferating ACs that retained their invasive abilities. Upon examination of the gene regulatory network controlling AC invasion, we determined that proliferating, invasive ACs maintain pro-invasive gene expression. We therefore report that maintenance of the post-mitotic state is not necessary for AC invasion, breaking the previously established C. elegans invasion/proliferation dichotomy.

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A NanoDam toolkit for tissue-specific transcription factor profiling inC. elegans

Cited by 4 publications

References 45 publications

EFL-3/E2F7 modulates Wnt signalling through repressing the LIT-1 Nemo-like kinase during asymmetric epidermal cell division inCaenorhabditis elegans

EFL-3/E2F7 modulates Wnt signalling through repressing the LIT-1 Nemo-like kinase during asymmetric epidermal cell division inCaenorhabditis elegans

An activity-regulated transcriptional program directly drives synaptogenesis

Cell cycle perturbation uncouples mitotic progression and invasive behavior in a post-mitotic cell

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