katch wreck"These data show that a reversible depletion of #Polycomb proteins can induce cancer in the absence of driver mutations, suggesting that tumours can emerge through #epigenetic dysregulation leading to inheritance of altered cell fates"
CavalliLabA nice paper is the best way to start the year: here evidence that the #Polycomb PRC1 complex is required to maintain the undifferentiated state of adult spermatogonia stem cells.
Nucleic Acids Res. 2023 Dec 24
doi: 10.1093/nar/gkad1203.
PRC1 directs PRC2-H3K27me3 deposition to shield adult spermatogonial stem cells from differentiation
Happy New Year: Peace, Joy, Health and Love for everybody !
In the paper below, exciting discussion on the evolution of #Polycomb complexes:
Uncoupled evolution of the Polycomb system and deep origin of non-canonical PRC1
Commun Biol. 2023 Nov 10;6(1):1144.
doi: 10.1038/s42003-023-05501-x
The EMBO JournalSeung Kim, Frederick Dick et al show that resting #Bcells are uniquely sensitive to #EZH2 #polycomb complex inhibition, which activates expression of repetitive genomic elements and subsequent #innateimmune receptor signaling in a form of viral mimicry
A universal #aging clock based on #DNA methylation profiles and linked to #Polycomb proteins:
doi: 10.1038/s43587-023-00462-6.
Universal DNA methylation age across mammalian tissues
The authors conclude: Our findings offer new evidence suggesting that aging is evolutionarily conserved and intertwined with developmental processes across all mammals.
A new study from Yuri Schwartz's lab:
#Polycomb proteins translate #histone #methylation to #chromatin
folding
DOI: 10.1016/j.jbc.2023.105080
Exciting work from Wendy Bickmore's lab on the relation between phase separation and #Polycomb:
Dispersal of PRC1 condensates disrupts polycomb chromatin domains and loops
doi: 10.26508/lsa.202302101.
Here the authors identify a protein that might promote cancer by inhibiting #Polycomb PRC2-mediated deposition of H3K27me3.
NOP16 is a histone mimetic that regulates Histone H3K27 methylation and gene repression
DOI: 10.1101/2023.06.13.544862
A famous #Polycomb protein with roles in gene silencing but also activation!
BMI1 fine-tunes gene repression and activation to safeguard undifferentiated spermatogonia fate
Front. Cell Dev. Biol., Volume 11 - 2023
BMI1 fine-tunes gene repression and activation to safeguard undifferentiated spermatogonia fate
Introduction: Spermatogenesis is sustained by the homeostasis of self-renewal and differentiation of undifferentiated spermatogonia throughout life, which is regulated by transcriptional and posttranscriptional mechanisms. B cell-specific Moloney murine leukemia virus integration site 1 (BMI1), one of spermatogonial stem cell markers, is a member of Polycomb repressive complex 1 (PRC1) and important to spermatogenesis. However, the mechanistic underpinnings of how BMI1 regulates spermatogonia fate remain elusive.Methods: We knocked down BMI1 by siRNA to investigate the role of BMI1 in undifferentiated spermatogonia. Differentially expressed genes were identified by RNA-seq and used for KEGG pathway analysis. We performed ChIP-seq analysis in wild type and BMI1 knockdown cells to explore the underlying molecular mechanisms exerted by BMI1. BMI1-associated alterations in repressive histone modifications were detected via Western blotting and ChIP-seq. Furthermore, we performed mass spectrometry and Co-immunoprecipitation assays to investigate BMI1 co-factors. Finally, we demonstrated the genomic regions occupied by both BMI1 and its co-factor.Results: BMI1 is required for undifferentiated spermatogonia maintenance by both repressing and activating target genes. BMI1 preserves PI3K-Akt signaling pathway for spermatogonia proliferation. Decrease of BMI1 affects the deposition of repressive histone modifications H2AK119ub1 and H3K27me3. BMI also positively regulates H3K27ac dep...