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Stutzman, A.

Publications and source records attributed to Stutzman, A..

2 recordsLinked to original sources

Early postpartum development of pup urine preference in mothers

The transition to motherhood involves profound physiological and neural changes, including adaptations in the sensory systems that support infant care.1,2 While the olfactory system plays a critical role in guiding maternal behaviors such as pup retrieval and nesting,3,4 how olfactory processing itself is reshaped during motherhood remains poorly understood. Here, we show that first-time mothers develop a selective preference for pup urine following parturition and early postpartum care, a preference not observed for other social or neutral odors. Using odor preference assays combined with liquid and gas chromatography-mass spectrometry, we identify specific volatile compounds in pup urine that may contribute to this maternal attraction. Disruption of olfactory input or restriction of contact chemosensation abolished the preference, indicating that both volatile and non-volatile sensory modalities contribute, likely through combined input from the main olfactory epithelium (MOE) and vomeronasal organ (VNO).5,6 Notably, this preference is absent in late-pregnant females, in mothers separated from pups at birth, and in virgins cohoused with pups or exposed to pup urine-highlighting that pup urine preference depends on the convergence of internal hormonal signals and external chemosensory cues.7,8 These findings reveal a previously unrecognized specificity in maternal olfactory behavior and provide insight into how motherhood modulates the sense of smell to support offspring recognition and care. In BriefMaternal pup urine preference depends on both hormonal changes and chemosensory cues associated with motherhood. HighlightsO_LIPup urine specifically attracts postpartum mothers but not virgin females C_LIO_LIPup urine contains distinct volatile and non-volatile metabolites C_LIO_LIPup urine preference requires both pup experience and the hormonal priming of motherhood C_LI

neuroscience↗

The cGAS-STING pathway is dispensable in a mouse model of LMNA-cardiomyopathy despite nuclear envelope rupture

Nuclear envelope (NE) ruptures are emerging observations in Lamin-related dilated cardiomyopathy, an adult-onset disease caused by loss-of-function mutations in Lamin A/C, a nuclear lamina component. Here, we tested a prevailing hypothesis that NE ruptures trigger pathological cGAS-STING cytosolic DNA-sensing pathway, using a mouse model of Lamin-cardiomyopathy. Reduction of Lamin A/C in cardiomyocytes of adult mice caused pervasive NE ruptures in cardiomyocytes, preceding inflammatory transcription, fibrosis, and fatal dilated cardiomyopathy. NE ruptures were followed by DNA damage accumulation without causing immediate cardiomyocyte death. However, cGAS-STING-dependent inflammatory signaling remained inactive. Deleting cGas or Sting did not rescue cardiomyopathy. The lack of cGAS-STING activation was likely due to the near absence of cGAS expression in adult cardiomyocytes at baseline. Instead, extracellular matrix (ECM) signaling was activated and predicted to initiate pro-inflammatory communication from Lamin-reduced cardiomyocytes to fibroblasts. Our work nominates ECM signaling, not cGAS-STING, as a potential inflammatory contributor in Lamin-cardiomyopathy.

molecular biology↗