Anushweta Asthana

All Publications

• Synchronized temporal-spatial analysis via microscopy and phosphoproteomics (STAMP) of quiescence. Science advances Azizzanjani, M. O., Turn, R. E., Asthana, A., Linde-Garelli, K. Y., Xu, L. A., Labrie, L. E., Mobedi, M., Jackson, P. K. 2025; 11 (17): eadt9712

  Abstract

  Coordinated cell cycle regulation is essential for homeostasis, with most cells in the body residing in quiescence (G0). Many pathologies arise due to disruptions in tissue-specific G0, yet little is known about the temporal-spatial mechanisms that establish G0 and its signaling hub, primary cilia. Mechanistic insight is limited by asynchronous model systems and failure to connect context-specific, transient mechanisms to function. To address this gap, we developed STAMP (synchronized temporal-spatial analysis via microscopy and phosphoproteomics) to track changes in cellular landscape occurring throughout G0 transition and ciliogenesis. We synchronized ciliogenesis and G0 transition in two cell models and combined microscopy with phosphoproteomics to order signals for further targeted analyses. We propose that STAMP is broadly applicable for studying temporal-spatial signaling in many biological contexts. The findings revealed through STAMP provide critical insight into healthy cellular functions often disrupted in pathologies, paving the way for targeted therapeutics.

  View details for DOI 10.1126/sciadv.adt9712

  View details for PubMedID 40279433

• Ciliary localization of GPR75 promotes fat accumulation in mice JOURNAL OF CLINICAL INVESTIGATION Chavez, M., Asthana, A., Jackson, P. K. 2024; 134 (19)

  Abstract

  Obesity is a growing public health concern that affects the longevity and lifestyle of all human populations including children and older individuals. Diverse factors drive obesity, making it challenging to understand and treat. While recent studies highlight the importance of GPCR signaling for metabolism and fat accumulation, we lack a molecular description of how obesogenic signals accumulate and propagate in cells, tissues, and organs. In this issue of the JCI, Jiang et al. utilized germline mutagenesis to generate a missense variant of GRP75, encoded by the Thinner allele, which resulted in mice with a lean phenotype. GPR75 accumulated in the cilia of hypothalamic neurons. However, mice with the Thinner allele showed defective ciliary localization with resistance to fat accumulation. Additionally, GPR75 regulation of fat accumulation appeared independent of leptin and ADCY3 signaling. These findings shed light on the role of GPR75 in fat accumulation and highlight the need to identify relevant ligands.

  View details for DOI 10.1172/JCI185059

  View details for Web of Science ID 001333356000013

  View details for PubMedID 39352389

  View details for PubMedCentralID PMC11444157