Located on Busch Campus of Rutgers, The State University of New Jersey, the Waksman Institute of Microbiology is an interdisciplinary research institute devoted to excellence in basic research. Focus areas include developmental biology, cell biology, biochemistry, structural biology, genetics, and genomics.

To support the educational mission of Rutgers, Waksman faculty members hold appointments in academic departments throughout the university. Our researchers train undergraduate students, graduate students, and post-doctoral fellows, as well as engage high school students in research through an outreach program.

Recent Publications

Mao, Y, Francis-West P, Irvine KD.  2015.  A Fat4-Dchs1 signal between stromal and cap mesenchyme cells influences nephrogenesis and ureteric bud branching.. Development (Cambridge, England). AbstractWebsite
Formation of the kidney requires reciprocal signaling among the ureteric tubules, cap mesenchyme and surrounding stromal mesenchyme to orchestrate complex morphogenetic events. The protocadherin Fat4 influences signaling from stromal to cap mesenchyme cells to influence their differentiation into nephrons. Here we characterize the role of a putative binding partner of Fat4, the protocadherin Dchs1. Mutation of Dchs1 leads to increased numbers of cap mesenchyme cells, which are abnormally arranged around the ureteric bud tips, and impairs nephron morphogenesis. Mutation of Dchs1 also reduces branching of the ureteric bud and impairs differentiation of ureteric bud tip cells into trunk cells. Genetically, Dchs1 is required specifically within cap mesenschyme cells. The similarity of Dchs1 phenotypes to stromal-less kidneys and to Fat4 mutants implicate Dchs1 in Fat4-dependent stroma-to-cap mesenchyme signaling. Antibody staining of genetic mosaics reveals that Dchs1 protein localization is polarized within cap mesenchyme cells, where it accumulates at the interface with stromal cells, implying that it interacts directly with a stromal protein. Our observations identify a role for Fat4-Dchs1 in signaling between cell layers, implicate Dchs1 as a Fat4 receptor for stromal signaling that is essential for kidney development, and establish that vertebrate Dchs1 can be molecularly polarized in vivo.
Durst, R, Peal DS, deVlaming A, Leyne M, Talkowski M, Perrocheau M, Simpson C, Jett C, Stone MR, Charles F et al..  2015.  Mutations in DCHS1 Cause Mitral Valve Prolapse. Nature. :inpress.
Irvine, KD, Harvey KF.  2015.  Control of organ growth by patterning and hippo signaling in Drosophila.. Cold Spring Harbor perspectives in biology. 7 AbstractWebsite
Control of organ size is of fundamental importance and is controlled by genetic, environmental, and mechanical factors. Studies in many species have pointed to the existence of both organ-extrinsic and -intrinsic size-control mechanisms, which ultimately must coordinate to regulate organ size. Here, we discuss organ size control by organ patterning and the Hippo pathway, which both act in an organ-intrinsic fashion. The influence of morphogens and other patterning molecules couples growth and patterning, whereas emerging evidence suggests that the Hippo pathway controls growth in response to mechanical stimuli and signals emanating from cell-cell interactions. Several points of cross talk have been reported between signaling pathways that control organ patterning and the Hippo pathway, both at the level of membrane receptors and transcriptional regulators. However, despite substantial progress in the past decade, key questions in the growth-control field remain, including precisely how and when organ patterning and the Hippo pathway communicate to control size, and whether these communication mechanisms are organ specific or general. In addition, elucidating mechanisms by which organ-intrinsic cues, such as patterning factors and the Hippo pathway, interface with extrinsic cues, such as hormones to control organ size, remain unresolved.