That sounds soooo exciting! Yes, the thrill of looking at the past is truly exciting, but the process of discovery is slow, tedious, and frustrating, especially when nothing is found.
This article has been cited by other articles in PMC. Abstract Genetically engineered mice have provided much information about gene function in the field of developmental biology.
The increase in number of kidney-specific Cre mice allows for the analysis of phenotypes Mari hilgers cannot be addressed by conventional gene targeting. The mammalian kidney is a vital organ that plays a critical homeostatic role in the regulation of body fluid composition and excretion of waste products.
The interactions between epithelial and mesenchymal cells are very critical events in the field of developmental biology, especially renal development. Kidney development is a complex process, requiring inductive interactions between epithelial and mesenchymal cells that eventually lead to the growth and differentiation of multiple highly specialized Mari hilgers, vascular, and epithelial cell types.
Through the use of genetically engineered mouse models, the molecular bases for many of the events in the developing kidney have been identified. Defective morphogenesis may result in clinical phenotypes that range from complete renal agenesis to diseases such as hypertension that exist in the setting of grossly normal kidneys.
In this review, we focus on the growth and transcription factors that define kidney progenitor cell populations, initiate ureteric bud branching, induce nephron formation within the metanephric mesenchyme, and differentiate stromal and vascular progenitors in the metanephric mesenchyme.
The reciprocal inductive interactions between epithelial cells and adjacent mesenchymal cells are of particular importance during embryogenesis, because they result in cellular differentiation and the formation of tissues and organs.
Specifically, in kidney development, the organization of polarized mesenchyme into epithelialized tubules is a characteristic feature, and is central to its physiological functions.
Overall, kidney morphogenesis appears as a self-regulating process, whereby kidney function orchestrates multiple, mutually dependent cellular processes within the developing nephron [ 1 ]. In recent years, the application of new techniques to study the genes or factors involved in renal morphogenesis has represented a key advancement in nephrology, leading to better understanding of renal development during prenatal and postnatal life [ 2 ].
These techniques have also provided important insights into the mechanisms of diseases that result from alteration of the morphogenesis program [ 3 ].
In this review, we focus on molecular pathways that regulate the process of mesenchyme-to-epithelial transition METthe main development responsible for the origin of the nephron, the functional unit of the kidney. Progress in our understanding of the cellular and molecular mechanisms of kidney development may provide methods for the improved diagnosis of renal anomalies and targets for the prevention and treatment of kidney disease.
Kidney-specific Gene Targeting Genetic engineering in mice has proven to be a useful tool for assessing the role of specific gene products in renal health and disease.
Cre recombinase cyclization recombination is a site-specific DNA recombinase from bacteriophage P1 that mediates genetic recombination at specific 34 bp recognition sites, called loxP [ 4 ].
As illustrated in Fig. The success of kidney-specific targeting is dependent on the availability of different Cre transgenic lines and the efficiency of the lineage-specific DNA excision. There are a number of kidney-specific Cre mouse strains currently available, which potentially allow for gene targeting in the podocyte, proximal tubule PTthick ascending limbs, juxtaglomerular cells, principle cells, and intercalated cells of the collecting duct [ 56 ].
Much of this early work in kidney development is summarized in a classic monograph by Saxen and Sariola [ 7 ].
In recent years, new techniques have given us outlines of the genetic program that regulates organogenesis and suggested roles for several signaling molecules, growth factors, receptors, transcription factors, and extracellular matrix com ponents.Doctor Profile: Tara Lynn Wenger, MD.
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Essential Alumni | Class Rosters. Christine Bailie Jonathan Barona Nicole Bell Lynn Boswell Keffrelyn Brown Mari Robinson Rey Rodriguez Steve Roth Kali’ Rourke Sue Runnells Michael Slack Russell Smith* Paul Hilgers Johanne Ibsen-Wolford Jim Innes Joia Jitahidi Iris Jones Jeff Latimer Susan Longley Judy Loredo.
Overall Finish List - Girls: 6A Varsity Girls: O'All Place. Adj Place. Bib No. Name: Team: Time. Pace.
Year. 1. 1. Miah Nelson: Odessa Permian: Catherine M Reins • Dawn Thompson Hilgers • Jodi Lynn Hilgers • Hilgers Alfred • John Alfred Hilgers • Mari Hilgers.
Show all locations and family. View details; Age 80+ Don E Hilgers. Rolla MO Other Locations. Saint Louis MO San Francisco CA Springfield MO Family. Pat A Hilgers.