Many diseases of the kidney stem from disruptions to the transcriptional programs involved in normal kidney development 
. Such disruptions, resulting from both genetic and environmental factors, can affect overall renal function in postnatal life. Indeed, predisposition to renal disease in humans is inversely related to the number of functional epithelial nephrons per kidney 
, a parameter completely determined during kidney development. Understanding this molecular pathogenesis has been a major aim of kidney organogenesis research 
. To do this, it is critical to understand the extent and origins of cellular complexity within the developing kidney.
Kidney organogenesis in mammalian species is highly conserved anatomically and molecularly. Hence, the field has made considerable use of model organisms, predominantly mouse and rat, to study the process. The mammalian kidney is a complex organ containing more than 25 distinct functional cell types 
. These arise from one of two intermediate mesoderm-derived cell populations, the metanephric mesenchyme (MM) and the ureteric bud 
. The UB forms a dichotomously branching epithelial tree, giving rise to the cell types that make up the collecting ducts of the kidney and the ureter that connects the kidney with the bladder. This involves considerable regional specification to ensure the vast variation in water permeability between the water-reclaiming collecting ducts and the water impermeable conduit that is the ureter. Regionalisation within this compartment is also critical for nephron formation as key proteins expressed by the tips of this epithelium signal to the surrounding mesenchyme to initiate nephrogenesis. Equally, there is now evidence that the segmentation and patterning of the nephrons themselves is dictated via the secretion of distinct Wnt proteins from the collecting duct tree 
. The MM gives rise to the cap mesenchyme (CM), which in turn forms all of the tubular elements of the nephron other than the collecting ducts via a process of mesenchyme to epithelial transition (MET) immediately adjacent to the tip of the advancing UB branches 
. As a result, the human kidney forms up to 2 million nephrons per kidney. An individual mature nephron is comprised of at least 14 distinct functional segments 
, each of which contains cell types that play specific roles in water and solute retention and loss. While patterning and segmentation must occur to reach this level of specialization, only the earliest events have been well studied. Hence the role of Wnt9b
in the initiation of MET and the subsequent requirement for Wnt4
expression to proceed through this event is well documented 
, as is the requirement for Notch2
for proximal tubule specification 
. The regulation of subsequent events remains to be dissected. The remainder of the MM does not undergo MET, instead giving rise to elements of the interstitium of the kidney. The interstitium as a whole is highly heterogeneous, containing fibroblasts, resident macrophages, vascular, perivascular/smooth muscle, lymphatic and neural tissue of the kidney 
. While some interstitial cell types are likely to migrate into the interstitium during development, including the resident macrophages/dendritic cells 
, the origin and lineage relationships of these components is still unresolved, as are their roles during normal kidney homeostasis and in response to renal injury 
The development of conditional transgenic strains in the mouse has particularly assisted in defining our existing understanding of ontological relationships during kidney development. For example, the Six2
gene is regionally-enriched in the CM during kidney development 
. Using a Six2GFPCre transgenic line, Kobayashi et al (2008) demonstrated that all epithelial portions of the nephron apart from the collecting duct were derived from CM 
. Using the same transgenic line, it was shown that during renal injury no interstitial stem cells could contribute to tubular repair as there is no apparent dilution of the nephron epithelium with cells that did not originally express Six2 
. Finally, Georgas et al (2009) showed that the connecting segment cells at the point of fusion between the collecting duct tips and the nephron tubules are derived from the CM and not the UB 
. The power of these analyses rests with the compartment-specific expression of the Six2
gene. The identification of additional compartment-specific genes is needed to advance our understanding of kidney development, notably during the later stages of patterning, segmentation and differentiation. The obvious solution to this would appear to be gene expression analysis of kidney development.
While global analysis of gene expression in the entire developing kidney has been of limited value given the cellular complexity of this organ 
, we have previously contributed to the most comprehensive compartmental analysis of any developing organ, in which Affymetrix microarray expression profiling was performed on 15 distinct temporospatial anatomical compartments of the developing mouse kidney collected via laser capture micro-dissection or FACS 
. This allowed for the identification of genes and gene networks enriched during different processes of kidney development, but also highlighted the paucity of genes absolutely restricted in expression to a single compartment in time and space.
Microarray compartments in Brunskill et al (2008) 
were based primarily upon identifiable anatomical and/or regional subdivisions rather than established molecular or ontological entities. Other gene expression studies during organogenesis 
have demonstrated the need for complimentary high resolution validation to more finely dissect the relationship between gene expression and anatomical organization. It was anticipated that this would reveal additional ‘molecularly-defined’ compartments more representative of key developmental processes, including segmentation and patterning, and possibly also identify specific cell types within complex and heterogeneous compartments. In the study presented here, we have extended the analysis of the kidney development gene atlas using high resolution section in situ
hybridisation (SISH). A bioinformatic method was devised for the stringent prediction of ‘anchor’ genes, defined as a gene whose expression was restricted to one temporospatial anatomical compartment. A total of 200 genes across 11 anatomical compartments were analysed with 46% of genes (92 genes) being compartment-enriched and an additional 18.5% (37 genes) representing anchor genes for a defined temporospatial structure (overall validation of bioinformatic selection of 64.5%). As such, these anchor genes will fuel the generation of further mouse resources for lineage tracing, thereby extending our understanding of kidney organogenesis and ultimately molecular pathogenesis within the kidney. Equally, compartment-enriched genes redefined the developing kidney atlas into molecular events rather than regional or anatomical structures, identifying markers able to subdivide the processes of nephron segmentation, collecting duct functionalisation and interstitial differentiation.