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Lee, Kiho,Kwon, Deug-Nam,Ezashi, Toshihiko,Choi, Yun-Jung,Park, Chankyu,Ericsson, Aaron C.,Brown, Alana N.,Samuel, Melissa S.,Park, Kwang-Wook,Walters, Eric M.,Kim, Dae Young,Kim, Jae-Hwan,Franklin, C National Academy of Sciences 2014 PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF Vol.111 No.20
<P>Pigs with severe combined immunodeficiency (SCID) may provide useful models for regenerative medicine, xenotransplantation, and tumor development and will aid in developing therapies for human SCID patients. Using a reporter-guided transcription activator-like effector nuclease (TALEN) system, we generated targeted modifications of recombination activating gene (<I>RAG</I>) 2 in somatic cells at high efficiency, including some that affected both alleles. Somatic-cell nuclear transfer performed with the mutated cells produced pigs with <I>RAG2</I> mutations without integrated exogenous DNA. Biallelically modified pigs either lacked a thymus or had one that was underdeveloped. Their splenic white pulp lacked B and T cells. Under a conventional housing environment, the biallelic <I>RAG2</I> mutants manifested a “failure to thrive” phenotype, with signs of inflammation and apoptosis in the spleen compared with age-matched wild-type animals by the time they were 4 wk of age. Pigs raised in a clean environment were healthier and, following injection of human induced pluripotent stem cells (iPSCs), quickly developed mature teratomas representing all three germ layers. The pigs also tolerated grafts of allogeneic porcine trophoblast stem cells. These SCID pigs should have a variety of uses in transplantation biology.</P>
Structural Basis for Assembly and Function of a Heterodimeric Plant Immune Receptor
Williams, Simon J.,Sohn, Kee Hoon,Wan, Li,Bernoux, Maud,Sarris, Panagiotis F.,Segonzac, Cecile,Ve, Thomas,Ma, Yan,Saucet, Simon B.,Ericsson, Daniel J.,Casey, Lachlan W.,Lonhienne, Thierry,Winzor, Dona American Association for the Advancement of Scienc 2014 Science Vol.344 No.6181
<P><B>Universal Immune Function</B></P><P>Certain pathogen effectors are detected in plants by cytoplasmic receptors. First solving the crystal structures of <I>Arabidopsis</I> receptors, <B>Williams <I>et al.</I></B> (p. 299; see the Perspective by <B>Nishimura and Dangl</B>) discovered that in the resting state, the structures form a heterodimer that readies the complex for effector binding and keeps the signaling domains from firing too early. Once the pathogen effector binds, the structure of the complex shifts such that the signaling domains can form a homodimer to initiate downstream signaling. Similarities between these plant-pathogen receptors and Toll-like receptors in animals suggest the molecular mechanisms may translate broadly.</P>