Michalis Barkoulas

This study shows that HDAC1/2-mediated repression of Wnt receptors orients asymmetric division polarity in C. elegans seam cells by establishing positional cues.

This study identifies CDC-37 as a regulator of oomycete immunity in C. elegans by controlling FLOR-1 localization and function through the CDC-37/HSP-90 complex.

The paper identifies transcriptional asymmetry in Wnt pathway components during C. elegans seam cell divisions, revealing feedback mechanisms that reinforce cell fate decisions.

This paper identifies two C-type lectin receptor pairs in C. elegans that mediate recognition of specific oomycete pathogens and show they are co-regulated and function redundantly in host defense.

This study shows EFL-3 represses LIT-1/NLK to modulate Wnt signaling during asymmetric epidermal cell division in C. elegans.

The paper infers the core gene regulatory network governing seam cell development in C. elegans using smFISH data and computational models.

The paper introduces NanoDam, a method for tissue-specific transcription factor profiling in C. elegans using endogenous GFP-tagged TFs and nanobody-Dam fusions, identifying novel targets in specific cell types.

The paper introduces Targeted DamID (TaDa) to identify tissue-specific transcription factor targets in C. elegans and validates its use in studying LIN-22 and NHR-25 in epidermal cell differentiation.

The paper shows that a single amino acid deletion in the heat shock protein HSP-110 in the C. elegans isolate CB4856 reduces the expressivity of a mutation in egl-18.

The paper shows that increased temperature causes a cell fate switch in C. elegans seam cells through changes in the Wnt asymmetry pathway, leading to symmetric cell divisions and increased seam cell numbers.

The paper introduces a CDK sensor to distinguish cycling cells from terminally differentiated cells in C. elegans and zebrafish, revealing commitment points and stochasticity in cell cycle control.

This study identifies two C. elegans-specific genes, pals-22 and pals-25, which function as antagonistic regulators controlling the switch between growth and pathogen resistance.