Revalidation of Myotis taiwanensis Arnback-Christie-Linde 1908 and its molecular relationship with M. adversus (Horsfield 1824) (Vespertilionidae, Chiroptera)
ACTA CHIROPTEROLOGICA
Authors: Han, Nai-Jian; Zhang, Jin-Shuo; Reardon, Terry; Lin, Liang-Kong; Zhang, Jun-Peng; Zhang, Shu-Yi
Abstract
A combined approach using molecular and morphological data has revealed that the taxon Myotis taiwanensis, which until now has been,usually considered as a subspecies of Myotis adversus, should be reinstated as a full species, as originally described by Arnback-Christie-Linde (1908) from Takao, Anping, Tainan, Formosa (= southern Taiwan). In our genetic analysis using two nuclear DNA segments of protein kinase C iota (PRKCI) and ubiquitin specific peptidase 9 (Usp9x), X-linked genes, together with two mitochondrial genes, i.e., nicotinamide adenine dinucleotide dehydrogenase subunit 1 (ND1) and cytochrome b (Cyt b), we demonstrate that M. taiwanensis is closely related to M pilosus, and largely divergent from two subspecies of M. adversus. Our analysis further shows that M. taiwanensis differs considerably from M. adversus in external and dental features. New records of M. taiwanensis from Shandong and Anhui provinces in eastern China are presented.
Chromosome 3q26 Gain Is an Early Event Driving Coordinated Overexpression of the PRKCI, SOX2, and ECT2 Oncogenes in Lung Squamous Cell Carcinoma
CELL REPORTS
Authors: Liu, Yi; Yin, Ning; Wang, Xue; Khoor, Andras; Sambandam, Vaishnavi; Ghosh, Anwesha B.; Fields, Zoe A.; Murray, Nicole R.; Justilien, Verline; Fields, Alan P.
Abstract
Lung squamous cell carcinoma (LSCC) is a prevalent form of lung cancer exhibiting distinctive histological and genetic characteristics. Chromosome 3q26 copy number gain (CNG) is a genetic hallmark of LSCC present in >90% of tumors. We report that 3q26 CNGs occur early in LSCC tumorigenesis, persist during tumor progression, and drive coordinate overexpression of PRKCI, SOX2, and ECT2. Over-expression of PRKCI, SOX2, and ECT2 in the context of Trp53 loss is sufficient to transform mouse lung basal stem cells into tumors with histological and genomic features of LSCC. Functionally, PRKCI and SOX2 collaborate to activate an extensive transcriptional program that enforces a lineage-restricted LSCC phenotype, whereas PRKCI and ECT2 collaborate to promote oncogenic growth. Gene signatures indicative of PKC iota-SOX2 and PKC iota-ECT2 signaling activity are enriched in the classical subtype of human LSCC and predict distinct therapeutic vulnerabilities. Thus, the PRKCI, SOX2, and ECT2 oncogenes represent a multigenic driver of LSCC.