Immediate lymphotoxin beta receptor-mediated transcriptional response in host defense against L. monocytogenes.

The lymphotoxin beta receptor (LTbetaR) mediates crucial signals in host defense against intracellular bacteria and viruses. Mice deficient in LTbetaR readily succumb to infections with Listeria monocytogenes, Mycobacterium tuberculosis and murine cytomegalovirus (mCMV). LTbetaR has been shown to be important for the early induction of interferon (IFN) beta after infection with mCMV.

Shedding of collagen XXIII is mediated by furin and depends on the plasma membrane microenvironment.

Collagen XXIII belongs to the class of type II orientated transmembrane collagens. A common feature of these proteins is the presence of two forms of the molecule: a membrane-bound form and a shed form. Here we demonstrate that, in mouse lung, collagen XXIII is found predominantly as the full-length form, whereas in brain, it is present mostly as the shed form, suggesting that shedding is tissue-specific and tissue-regulated.

Expression of type XXIII collagen mRNA and protein.

Collagen XXIII is a member of the transmembranous subfamily of collagens containing a cytoplasmic domain, a membrane-spanning hydrophobic domain, and three extracellular triple helical collagenous domains interspersed with non-collagenous domains. We cloned mouse, chicken, and humanalpha1(XXIII) collagen cDNAs and showed that this non-abundant collagen has a limited tissue distribution in non-tumor tissues. Lung, cornea, brain, skin, tendon, and kidney are the major sites of expression.

Formation of multiple hearts in mice following deletion of beta-catenin in the embryonic endoderm.

Using Cre/loxP, we conditionally inactivated the beta-catenin gene in cells of structures that exhibit important embryonic organizer functions: the visceral endoderm, the node, the notochord, and the definitive endoderm. Mesoderm formation was not affected in the mutant embryos, but the node was missing, patterning of the head and trunk was affected, and no notochord or somites were formed. Surprisingly, deletion of beta-catenin in the definitive endoderm led to the formation of multiple hearts all along the anterior-posterior (A/P) axis of the embryo.

E-cadherin is a survival factor for the lactating mouse mammary gland.

The Ca(++)-dependent cell adhesion molecule E-cadherin is expressed throughout mouse development and in adult tissues. Classical gene targeting has demonstrated that E-cadherin-deficient embryos die at the blastocyst stage. To study the involvement of E-cadherin in organogenesis, a conditional gene inactivation scheme was undertaken using the bacteriophage P1 recombinase Cre/loxP system.