Table of Contents
Research Articles
- SLX4IP and telomere dynamics dictate breast cancer metastasis and therapeutic responsiveness
An unbiased genetic screen established SLX4IP as an essential driver of telomere maintenance mechanism identity, metastatic progression, and therapeutic response of breast cancers.
- Splicing of enhancer-associated lincRNAs contributes to enhancer activity
Analysis of enhancer-associated lincRNA transcripts shows their efficient and conserved splicing contributes to cognate enhancer activity and cis-regulation of target gene expression.
- Keratinocyte interleukin-36 receptor expression orchestrates psoriasiform inflammation in mice
IL-36 stimulation of keratinocytes orchestrates key pathogenic inflammatory responses in psoriatic skin.
- Structures of SALSA/DMBT1 SRCR domains reveal the conserved ligand-binding mechanism of the ancient SRCR fold
The structures of SALSA SRCR domains 1 and 8 reveal a cation-dependent mechanism for ligand recognition, contributing to important roles in the immune system and cellular signalling. The cation-binding sites are conserved across all SRCR domains, suggesting conserved functional mechanisms.
- BACH family members regulate angiogenesis and lymphangiogenesis by modulating VEGFC expression
Our work highlights BACH family of transcription factors as a novel regulator of angiogenesis and lymphangiogenesis during zebrafish embryonic development and tumor expansion.
- CSDE1 controls gene expression through the miRNA-mediated decay machinery
CSDE1 is a new component of miRNA-induced silencing complex and interacts with DCP1–DCP2 decapping machinery with potential roles in miRNA-mediated target degradation.
- A novel class of polymorphic toxins in Bacteroidetes
Bacteria often use toxins to mediate their interaction with the environment. This study reveals a new class of polymorphic toxins, which contain an N-terminal TANFOR domain, in Bacteroidetes.
- Mylk3 null C57BL/6N mice develop cardiomyopathy, whereas Nnt null C57BL/6J mice do not
Genetic differences between C57BL/6 substrains lead to different cardiovascular traits; a null mutation in Mylk3 likely causes cardiomyopathy in C57BL/6N mice, whereas C57BL/6J Nnt-null mice do not develop cardiomyopathy.
Methods
- MagnEdit—interacting factors that recruit DNA-editing enzymes to single base targets
This study reports a new, non-covalent strategy—called MagnEdit—that attracts the DNA cytosine deaminase APOBEC3B to a Cas9-directed site for C-to-T editing.
- Simultaneous multiple allelic replacement in the malaria parasite enables dissection of PKG function
This work combines the use of an inducible Cre recombinase and different lox sites to simultaneously create multiple allelic replacements. We show that an essential malarial cGMP-dependent protein kinase functions exclusively during the release of the parasite from its host cell.