Here, we described Gekko (Japonigekko) ichangensis sp. nov., a new member of the genus Gekko Laurenti, 1768, based on specimens collected from Changyang Tujia Autonomous County, Yichang City, Hubei Province, China. Morphological comparisons and phylogenetic analyses using mitochondrial cytb and 16S genes place the new species within the subgenus Japonigekko, clustering with G. (J.) wenxianensis. The new species differs from other Japonigekko congeners by the following set of characteristics: (1) moderate body size (snout-vent length 58.5–66.5 mm in adult individuals); (2) nostrils touching the rostral, with 1–2 internasals present; (3) tubercles distributed on the head, dorsum, limbs, and tail, excluding the upper forelimbs; (4) 174–195 ventral scales spanning from the mental to the cloacal slit; (5) 39–47 rows of ventral scales; (6) 12–15 subdigital lamellae under the first toes and 13–18 under the fourth toes; (7) weakly developed webbing; (8) 5–8 precloacal pores in males; (9) three unilateral postcloacal tubercles; (10) a brown dorsum with six broad, irregular dark-brown bands extending from the nape to the sacrum. The identification of this new species raises the number of described Gekko species to 90. In China, 26 species are recorded, 21 of which belong to the subgenus Japonigekko.

Mouse zygotes undergo multiple rounds of cell division, resulting in the formation of preimplantation blastocysts comprising three lineages: trophectoderm (TE), epiblast (EPI), and primitive endoderm (PrE). Cell fate determination plays a crucial role in establishing a healthy pregnancy. The initial separation of lineages gives rise to TE and inner cell mass (ICM), from which trophoblast stem cells (TSC) and embryonic stem cells (ESC) can be derived in vitro. Studying lineage differentiation is greatly facilitated by the clear functional distinction between TSC and ESC. However, transitioning between these two types of cells naturally poses challenges. In this study, we demonstrate that inhibiting LATS kinase promotes the conversion of ICM to TE and also effectively reprograms ESC into stable, self-renewing TS-like cells (TSLC). Compared to TSC, TSLC exhibits similar molecular properties, including the high expression of marker genes such as Cdx2, Eomes, and Tfap2c, as well as hypomethylation of their promoters. Importantly, TSLC not only displays the ability to differentiate into mature trophoblast cells in vitro but also participates in placenta formation in vivo. These findings highlight the efficient reprogramming of ESCs into TSLCs using a small molecular inducer, which provides a new reference for understanding the regulatory network between ESCs and TSCs.

Background: Pancreatic ductal adenocarcinoma (PDAC) is a lethal malignancy with a five-year survival rate of approximately 10%. Genetic mutations are pivotal drivers in PDAC pathogenesis, but recent investigations also revealed the involvement of non-genetic alterations in the disease development. In this study, we undertook a multi-omics approach, encompassing ATAC-seq, RNA-seq, ChIP-seq, and Hi-C methodologies, to dissect gene expression alterations arising from changes in chromosome accessibility and chromatin three-dimensional interactions in PDAC. Results: Our findings indicate that chromosomal structural alterations can lead to abnormal expressions on key genes during PDAC development. Notably, overexpression of oncogenes FGFR2, FOXA2, CYP2R1, and CPOX can be attributed to the augmentation of promoter accessibility, coupled with long-range interactions with distal elements. Additionally, our findings indicate that chromosomal structural alterations caused by genomic instability can lead to abnormal expressions in PDACs. As an example, by analyzing chromosomal changes, we identified a putative oncogenic gene, LPAR1, which shows upregulated expression in both PDAC cell lines and clinical samples. The overexpression is correlated with alterations in LPAR1-associated 3D genome structure and chromatin state. We further demonstrated that high LPAR1 activity is required for enhanced PDAC cell migration in vitro. Conclusions: Collectively, our findings reveal that the chromosomal conformational alterations, in addition to the well-known genetic mutations, are critical for PDAC tumorigenesis.

Vasa, an RNA binding protein with an ATP-dependent helicase domain, is one of the critical germ cell factors. In this study, we reported cloning of a full-length vasa cDNA from tree frog F. palpebralis. The predicated F. palpebralis Vasa shares eight conserved regions with Vasa proteins from other vertebrates. Furthermore, we confirmed germline specific expression of the vasa RNA by RT-qPCR. These results suggest that vasa is involveed in germ cell specification in F. palpebralis. Our observation provides a new tool to study germ cell formation in amphibians.