This is a pre-copyedited, author-produced PDF of an article accepted for publication in Monthly Notices of the Royal Astronomical Society following peer review. The version of record Barragán, O. et al. "K2-139 b: A low-mass warm Jupiter on a 29-d orbit transiting an active K0 V star" is available online at: http://doi.org/10.1093/mnras/stx3207 ; We announce the discovery of K2-139 b (EPIC 218916923 b), a transiting warm-Jupiter (Teq= 547± 25 K) on a 29-d orbit around an active (logR'HK=-4.46±0.06) K0V star in K2 Campaign 7.We derive the system's parameters by combining the K2 photometry with groundbased follow-up observations. With a mass of 0.387-0.033+0.075MJand radius of 0.808-0.033+0.034RJ, K2-139 b is one of the transiting warm Jupiters with the lowest mass known to date. The planetary mean density of 0.91-0.20+0.24g cm-3can be explained with a core of ~50M⊕. Given the brightness of the host star (V=11.653 mag), the relatively short transit duration (~5 h), and the expected amplitude of the Rossiter-McLaughlin effect (~25m s-1), K2-139 is an ideal target to measure the spin-orbit angle of a planetary system hosting a warm Jupiter ; D. Gandolfi gratefully acknowledges the financial support of the Programma Giovani Ricercatori – Rita Levi Montalcini – Rientro dei Cervelli (2012) awarded by the Italian Ministry of Education, Universities and Research (MIUR). Sz. Csizmadia thanks the Hungarian OTKA Grant K113117. H. J. Deeg and D. Nespral acknowledge support by grant ESP2015-65712-C5-4-R of the Spanish Secretary of State for R& D&i (MINECO). D. Lorenzo-Oliveira acknowledges the support from FAPESP (2016/20667-8). This research was supported by the Ministerio de Economia y Competitividad under project FIS2012-31079. The research leading to these results has received funding from the European Union Seventh Framework Programme (FP7/2013-2016) under grant agreement No. 312430 (OPTICON).
Mutations affecting spliceosomal proteins are the most common mutations in patients with myelodysplastic syndromes (MDS), but their role in MDS pathogenesis has not been delineated. Here we report that mutations affecting the splicing factor SRSF2 directly impair hematopoietic differentiation in vivo, which is not due to SRSF2 loss of function. By contrast, SRSF2 mutations alter SRSF2's normal sequence-specific RNA binding activity, thereby altering the recognition of specific exonic splicing enhancer motifs to drive recurrent mis-splicing of key hematopoietic regulators. This includes SRSF2 mutation-dependent splicing of EZH2, which triggers nonsense-mediated decay, which, in turn, results in impaired hematopoietic differentiation. These data provide a mechanistic link between a mutant spliceosomal protein, alterations in the splicing of key regulators, and impaired hematopoiesis. ; E.K. is supported by the Worldwide Cancer Research Fund. A.R. was supported by the NIH/NHLBI (U01 HL099993), NIH/NIDDK (K08 DK082783), the J.P. McCarthy Foundation, and the Storb Foundation. S.H. and O.A.-W. are supported by grants from the Edward P. Evans Foundation. S.H. was supported by Yale Comprehensive Cancer Center institutional funds. R.K.B. was supported by the Hartwell Innovation Fund, Damon Runyon Cancer Research Foundation (DFS 04-12), Ellison Medical Foundation (AG-NS-1030-13), NIH/NIDDK (R56 DK103854), NIH/NCI recruitment support (P30 CA015704), and Fred Hutchinson Cancer Research Center institutional funds. J.O.I. was supported by an NIH/NCI training grant (T32 CA009657) and NIH/NIDDK pilot study (P30 DK056465). C.L. is supported by a career development award grant from the Leukemia and Lymphoma Society and an ATIP-Avenir grant from the French government. O.A.-W. is supported by an NIH K08 clinical investigator award (1K08CA160647-01), a Department of Defense Postdoctoral Fellow Award in Bone Marrow Failure Research (W81XWH-12-1-0041), the Josie Robertson Investigator Program, and a Damon Runyon Clinical Investigator Award with support from the Evans Foundation. F.H.-T.A. acknowledges support from the NCCR RNA and Disease funded by the Swiss National Science Foundation and the SNF Sinergia CRSII3_127454. Y.L. and Y.M. were supported by NIH/NIGMS grant R01 GM102869 and Senior Research Fellowship Grant 101908/Z/13/Z (to Y.M.) from the Wellcome Trust. J.D. acknowledges assistance from Dr. Nezih Cereb, HistoGenetics (Ossining, NY). ; This is the author accepted manuscript. The final version is available from Elsevier via http://dx.doi.org/10.1016/j.ccell.2015.04.006