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Yang, X.-n.

Publications and source records attributed to Yang, X.-n..

2 recordsLinked to original sources

Ovipositor morphology and mechanosensory divergence drive niche breadth expansion in Drosophila

Ecological niche breadth is key factor associated with adaptive radiation and speciation. For most Drosophila species, the firm surface of intact ripe fruit acts as a physical barrier to oviposition, effectively restricting them to the saprophagous resources. How species overcome such mechanical constraints at the behavioral and sensory levels, and whether doing so leads to niche breadth expansion or niche specialization, remain poorly understood. Here, using comparative behavioral assays across ten Drosophila species, we show that substrate physical hardness is a critical barrier preventing most species from exploiting ripe fruit. Among species capable of puncture oviposition, there are two distinct evolutionary strategies among Drosophila species. With its serrated ovipositor and strong preference for fresh fruit, D. suzukii represents a case of ripe-fruit specialization. In contrast, D. immigrans with the needle-like ovipositor, gains access to fresh fruit while retaining the ability to exploit decaying substrates, thereby expanding its resource niche. Thus, D. suzukii considered as the typical evolutionary niche specialization, while D. immigrans represents niche expansion. Furthermore, using the genetic toolkit of D. melanogaster, we further identify the Inactive (IAV) mechanosensory channel as important regulator of stiffness-dependent oviposition inhibition. Loss of iav reduced inhibition on firm substrates, while cross-species rescue experiments showed that IAV orthologs differed in their ability to restore this response in a common genetic background. Puncture oviposition was also associated with successful offspring development on firm fruit and with the use of firm-surfaced hosts under natural conditions. Together, these findings identified a novel niche expansion of D. immigrans among the saprophagous Drosophila.

evolutionary biology↗

Hepatic Macrophage Migration Inhibitory Factor Promotes Pancreatic Cancer Liver Metastasis in NAFLD

How pathological livers shape tumors, thereby driving pancreatic ductal adenocarcinoma (PDAC) metastasis to the liver, is poorly understood. In the present study, we focus on examining key molecules implicated in this process and assessing their translational significance. We demonstrated that patients with combined non-alcoholic fatty liver disease (NAFLD) have approximately a ninefold increased risk of developing liver metastasis compared to those without NAFLD. In mice model, NAFLD fosters an immunosuppressive microenvironment with increased tumor cell pluripotency and focal adhesion. Mechanistically, NAFLD-induced MIF mediated the progression of PDAC liver metastasis by attracting CD44 positive pancreatic cells. Hepatic MIF knockdown significantly reduced metastases burden with decreased stem-like cancer cells, tumor associated macrophages (TAMs) infiltration and focal adhesion. Targeting the MIF-CD44 axis by either a MIF tautomerase inhibitor, IPG1576, or by CD44 knockdown in tumor cells significantly attenuate liver metastasis of PDAC within the NAFLD context. Patients with PDAC liver metastasis and NAFLD had elevated hepatic MIF expression and increased number of stem-cell like cancer cells. Collectively, our study highlights a pivotal role for MIF-CD44 axis in cancer stemness and offer novel avenues for tailoring therapeutic strategies to individual patients with NAFLD as an underlying condition.

cancer biology↗