Differential Notch Activity Is Required for Homeostasis of Malpighian Tubules in Adult Drosophila

Precise regulation of stem cell self-renewal versus differentiation is important for the maintenance of tissue ho- meostasis. Early loss of stem cell activity results in premature ageing, while excess stem cell activity leads to over- proliferation and cancer initiation （Fuchs et al., 2004; Scadden, 2006; Jones and Wagers, 2008; Morrison and Spradling, 2008）. Thus, understanding the mechanism con- trolling stem cell self-renewal and differentiation is critical for development of potential clinic therapy in the future.

Posterior gut development in Drosophila:a model system for identifying genes controlling epithelial morphogenesis

The posterior gut of the Drosophila embryo, consisting of hindgut and Malpighian tubules, provides a simple,well-defined system where it is possible to use a genetic approach to define components essential for epithelial morphogenesis.We review here the advantages of Drosophila as a model genetic organism, the morphogenesis of the epithelial structures of the posterior gut, and what is known about the genetic requirements to form these structures.In overview, primordia are patterned by expression of hierarchies of transcription factors; this leads to localized expression of cell signaling molecules, and finally, to the least understood step: modulation of cell adhesion and cell shape. We describe approaches to identify additional genes that are required for morphogenesis of these simple epithelia, particularly those that might play a structural role by affecting cell adhesion and cell shape.

EGFR/MAPK Signaling Regulates the Proliferation of Drosophila Renal and Nephric Stem Cells

Tissue homeostasis, accomplished through the self-renewai and differentiation of resident stem cells, is critical for the maintenance of adult tissues throughout an animal＇s lifetime, Adult Drosophila Malpighian tubules （MTs or fly kidney） are maintained by renal and nephric stem cells （RNSCs） via self-renewing divisions, however, it is unclear how RNSC proliferation and differentiation are regulated. Here we show that EGFR/MAPK signaling is dispensable for RNSC maintenance, but required for RNSC proliferation in vivo. Inacti- vation of the EGFR/MAPK pathway blocks or greatly retards RNSC cell cycle progression; conversely, over-activation of EGFR/MAPK signaling results in RNSC over-proliferation and disrupts the normal differentiation of renablasts （RBs）, the immediate daughters of RNSC divisions. Our data further suggest that EGFR/MAPK signaling functions independently of JAK/STAT signaling and that dMyc and CycE partially mediate EGFR/MAPK signaling in MTs. Together, our data suggest a principal role of EGFR/MAPK signaling in regulating RNSC proliferation, which may provide important clues for understanding mammalian kidney repair and regeneration following injury.