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February 21, 2025

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09/04/2025

research article

Spatial colocalization and molecular crosstalk of myofibroblastic CAFs and tumor cells shape lymph node metastasis in oral squamous cell carcinoma

In this study, the authors integrated bulk genome and transcriptome, single-cell transcriptome, and spatial transcriptome data from OSCC and found that myCAFs were quantitatively and functionally activated in LNM-positive samples and spatially colocalized with OSCC cells at the invasive tumor front, providing a niche that may facilitate LNM.

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Spatial colocalization and molecular crosstalk of myofibroblastic CAFs and tumor cells shape lymph node metastasis in oral squamous cell carcinoma

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Current Issue September 2025

08/26/2025

formal comment

On the role of the terminal oxidase cytochrome bd in hyper-resistance of Listeria monocytogenes to the macrodiolide antibiotic tartrolon B

This commentary discusses how the terminal oxidase cytochrome bd contributes to resistance of Listeria monocytogenes against the antibiotic tartrolon B. The authors outline evidence that cytochrome bd, but not cytochrome aa3, is required for resistance, and propose alternative models for how this oxidase helps maintain proton motive force and protect against the compound.

Image credit: pgen.1011803

On the role of the terminal oxidase cytochrome bd in hyper-resistance of Listeria monocytogenes to the macrodiolide antibiotic tartrolon B

08/14/2025

methods

Defining transcription factor nucleosome binding with Pioneer-seq

This study introduces Pioneer-seq, a method to examine transcription factor binding across thousands of nucleosomes. Using OCT4, SOX2, KLF4, and MYC, the authors show that all can bind at nucleosome edges and that nucleosome sequence is the primary factor regulating binding. KLF4 and SOX2 also bind near nucleosome centers, helping define the mechanistic requirements for pioneer factor binding.

Image credit: pgen.1011813

Defining transcription factor nucleosome binding with Pioneer-seq

09/02/2025

research article

Deficiency of Kif15 impairing synaptic development leads to mood disorder in mice

The authors show that Kif15 deficiency disrupts dendritic morphology and synaptic function in mice, contributing to mood disorder-like behaviors. Kif15-/- mice had reduced postsynaptic proteins and dendritic spines in adolescence, abnormal increases in adulthood, and overexpression of Kif15 rescued depressive behavior in zebrafish.

Deficiency of Kif15 impairing synaptic development leads to mood disorder in mice

Image credit: pgen.1011839

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PLOS Genetics | ISSN: 1553-7404 (online)