bioRxiv Science⌕ Search

Biology subjects

Akaki, K.

Publications and source records attributed to Akaki, K..

2 recordsLinked to original sources

The Tube-Sealing Test: A novel behavioral assay to quantify offspring-centered defensive behavior in postpartum mice

Perinatal mental health is a major public health concern, and postpartum women are particularly vulnerable to conditions such as postpartum obsessive-compulsive disorder and postpartum depression. Many postpartum symptoms involve heightened concern for infant safety, suggesting the presence of offspring-centered defensive processes that are distinct from general anxiety focused on self-safety. One offspring-centered defensive behavior described in wild rats is entrance-sealing, in which lactating females plug the entrance of their burrow to limit access by potential intruders. Although laboratory mice rarely exhibit sealing spontaneously, sealing-like behavior can be experimentally induced by chemogenetic activation of hypothalamic perifornical Urocortin-3 neurons, indicating that mice retain a latent motor pattern for this response. However, no method has existed for reliably quantifying sealing behavior under controlled laboratory conditions. To address this gap, we developed the Tube-Sealing Test (TST), an assay that measures bedding packed into tube-like openings attached to the home cage and enables repeated, non-invasive quantification of sealing behavior. Using this approach, we found that tube-sealing occurred rarely in males, intermittently in virgin females, and with markedly greater intensity in postpartum females. Although virgin and postpartum females showed a similar likelihood of performing sealing, postpartum females inserted substantially more bedding than either group. In postpartum females, exposure to a male intruder increased sealing specifically at the tube through which the intruder was introduced, indicating that sealing intensity is modulated by direct threat experience. Together, these findings establish the TST as a simple and reproducible method for quantifying sealing behavior and identify tube-sealing as a measurable component of offspring-centered defensive behavior.

animal behavior and cognition↗

IRAK1-dependent Regnase-1-14-3-3 complex formation controls Regnase-1-mediated mRNA decay

Regnase-1 is an endoribonuclease crucial for controlling inflammation by degrading mRNAs encoding cytokines and inflammatory mediators in mammals. However, it is unclear how Regnase-1-mediated mRNA decay is controlled in interleukin (IL)-1{beta} or Toll-like receptor (TLR) ligand-stimulated cells. Here, by analyzing the Regnase-1 interactome, we found that IL-1{beta} or TLR stimulus dynamically induced the formation of Regnase-1-{beta}-transducin repeat-containing protein ({beta}TRCP) complex. Importantly, we also uncovered a novel interaction between Regnase-1 and 14-3-3 in both mouse and human cells. Strikingly, both interactions occur in a mutually exclusive manner, underscoring the importance of modulating Regnase-1s activity. Additionally, we show that in IL-1R/TLR-stimulated cells, the Regnase-1-14-3-3 interaction is mediated by IRAK1 through a previously uncharacterized C-terminal structural domain. Phosphorylation of Regnase-1 at S494 and S513 is critical for Regnase-1-14-3-3 interaction, while a different set of phosphorylation sites of Regnase-1 are known to be required for the recognition by {beta}TRCP and proteasome-mediated degradation. 14-3-3 stabilizes Regnase-1 but abolishes its activity by inhibiting Regnase-1-mRNA association. Furthermore, nuclear-cytoplasmic shuttling of Regnase-1 is abrogated by 14-3-3 interaction. Taken together, the results suggest that a novel inflammation-induced interaction of 14-3-3 with Regnase-1 stabilizes inflammatory mRNAs by sequestering Regnase-1 in the cytoplasm to prevent mRNA recognition.

immunology↗