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Doerfel, K.

Publications and source records attributed to Doerfel, K..

2 recordsLinked to original sources

LIN-67 functionally interacts with heterochronic miRNAs and regulates developmental timing in Caenorhabditis elegans

Temporal regulation of gene expression is required for developmental transitions, including differentiation, proliferation, and morphogenesis. In the nematode Caenorhabditis elegans, heterochronic microRNAs (miRNAs) regulate the temporal expression of genes that promote animal development. The heterochronic miRNAs lin-4 and let-7 are required during different stages of larval development and are associated with the miRNA-specific Argonaute ALG-1. In this study, we have identified lin-67 as a heterochronic gene that negatively regulates lin-4, let-7, and alg-1. Loss of lin-67 function restores proper developmental timing and stage-specific gene expression to hypomorphic lin-4 and let-7 mutants. We found that loss of lin-67 resulted in a reduced number of seam cells, defects in alae formation, precocious expression of an adult-specific gene reporter, and sterility. LIN-67 contains a K homology (KH) RNA-binding domain and is a homolog of the Sam68-like splicing factor KHDRBS2. We show that LIN-67 localizes to the nucleus throughout animal development and is enriched in nuclear foci. Mutating the KH domain of LIN-67 abolished the nuclear localization of LIN-67, suggesting that the localization of LIN-67 is likely dependent on RNA-binding activity. We show that LIN-67 negatively regulates lin-4 miRNA levels and restores normal levels of let-7 to alg-1 mutants, which can, at least in part, explain how lin-67 suppresses alg-1. Our data indicate that lin-67 is a novel heterochronic gene that regulates developmental timing and miRNA-dependent gene regulation in C. elegans.

developmental biology↗

An Epigenetic Priming Mechanism Mediated by Nutrient Sensing Regulates Transcriptional Output

While 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 hours before transcriptional activation and by doing so, regulates both the duration and amplitude of subsequent target gene transcription. 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.

developmental biology↗