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Biology subjects

Stengel, S.

Publications and source records attributed to Stengel, S..

2 recordsLinked to original sources

UV laser crosslinking uncovers novel DNA-binding pattern of CTCF

Eukaryotic genomes are spatially organized to regulate gene expression, and CTCF is a key architectural protein that links chromatin topology to transcriptional control. Accurate mapping of CTCF-DNA interactions is critical for understanding gene regulation. However, conventional formaldehyde-based crosslinking in ChIP-seq biases towards long-lived protein-DNA interactions. We substituted chemical crosslinking with ultraviolet (UV) laser crosslinking (UV ChIP-seq) to capture both stable and dynamic CTCF-DNA interactions in living K-562 cells. UV ChIP-seq identified 38,706 CTCF binding sites, 70% of which were previously undetected by standard formaldehyde (FA) ChIP-seq. These UV-specific sites were enriched in active promoters, enhancers, and short-range chromatin loops, whereas formaldehyde ChIP-seq preferentially detected CTCF at topologically associated domain (TAD) boundaries and long-range loops. CTCF was detected at 85% of active transcription start sites, and when uniquely FA-identified sites were included, over 90% of active promoters were detected. De novo motif analysis also revealed noncanonical CTCF motifs at UV-specific sites, suggesting alternative binding configurations. These results expand the CTCF cistrome, redefine its role in active chromatin, and underscore the need for complementary crosslinking strategies to characterize the full spectrum of transcription factor-DNA interactions.

genomics↗

Leptin signaling regulates physiological damage and host-pathogen cooperation

To combat infections, hosts employ a combination of antagonistic and cooperative defense strategies. The former refers to pathogen killing mediated by resistance mechanisms, while the latter refers to physiological defense mechanisms that promote host health during infection independent of pathogen killing, leading to an apparent cooperation between the host and the pathogen. Previous work has shown that leptin, a pleiotropic hormone that plays a central role in regulating appetite and energy metabolism, is indispensable for resistance mechanisms, while a role for leptin signaling in cooperative host-pathogen interactions remains unknown. Using a mouse model of Yersinia pseudotuberculosis (Yptb) infection, the causative agent of Far East scarlet-like fever, we unexpectedly found that genetic inhibition of leptin signaling conferred protection from Yptb infection due to increased host-pathogen cooperation rather than greater resistance defenses. The protection against Yptb infection was not due to differences in food consumption, lipolysis or fat mass. Furthermore, we found that the survival advantage was associated with increased liver damage and dysfunction. Our work reveals an additional level of complexity for the role of leptin in infection defense and suggests that in some contexts, in addition to tolerating the pathogen, tolerating organ damage and dysfunction is more beneficial for survival than preventing the damage.

immunology↗