Fly最新文献

The model organism Drosophila melanogaster has become a focal system for investigations of rapidly evolving genital morphology as well as the development and functions of insect reproductive structures. To follow up on a previous paper outlining unifying terminology for the structures of the male terminalia in this species, we offer here a detailed description of the female terminalia of D. melanogaster. Informative diagrams and micrographs are presented to provide a comprehensive overview of the external and internal reproductive structures of females. We propose a collection of terms and definitions to standardize the terminology associated with the female terminalia in D. melanogaster and we provide a correspondence table with the terms previously used. Unifying terminology for both males and females in this species will help to facilitate communication between various disciplines, as well as aid in synthesizing research across publications within a discipline that has historically focused principally on male features. Our efforts to refine and standardize the terminology should expand the utility of this important model system for addressing questions related to the development and evolution of animal genitalia, and morphology in general.

Cell-cell interactions within tumour microenvironment play crucial roles in tumorigenesis. Genetic mosaic techniques available in Drosophila have provided a powerful platform to study the basic principles of tumour growth and progression via cell-cell communications. This led to the identification of oncogenic cell-cell interactions triggered by endocytic dysregulation, mitochondrial dysfunction, cell polarity defects, or Src activation in Drosophila imaginal epithelia. Such oncogenic cooperations can be caused by interactions among epithelial cells, mesenchymal cells, and immune cells. Moreover, microenvironmental factors such as nutrients, local tissue structures, and endogenous growth signalling activities critically affect tumorigenesis. Dissecting various types of oncogenic cell-cell interactions at the single-cell level in Drosophila will greatly increase our understanding of how tumours progress in living animals.

To maintain homoeostasis, cells must degrade damaged or misfolded proteins and synthesize functional replacements. Maintaining a balance between these processes, known as protein turnover, is necessary for stress response and cellular adaptation to a changing environment. Damaged mitochondria must also be removed and replaced. Changes in protein and mitochondrial turnover are associated with aging and neurodegenerative disease, making it important to understand how these processes occur and are regulated in cells. To achieve this, reliable assays of turnover must be developed. Several methods exist, including pulse-labelling with radioactive or stable isotopes and strategies making use of fluorescent proteins, each with their own advantages and limitations. Both cell culture and live animals have been used for these studies, in systems ranging from yeast to mammals. In vivo assays are especially useful for connecting turnover to aging and disease. With its short life cycle, suitability for fluorescent imaging, and availability of genetic tools, Drosophila melanogaster is particularly well suited for this kind of analysis.

Unregulated Ca²⁺ influx affects intracellular Ca²⁺ homoeostasis, which may lead to neuronal death. In Drosophila, following the activation of rhodopsin the TRP Ca²⁺ channel is open to mediate the light-dependent depolarization. A constitutively active TRP channel triggers the degeneration of Trp^P365 /+ photoreceptors. To explore retinal degeneration, we employed a multidisciplinary approach including live imaging using GFP tagged actin and arrestin 2. Importantly, we demonstrate that the major rhodopsin (Rh1) was greatly reduced before the onset of rhabdomere degeneration; a great reduction of Rh1 affects the maintenance of rhabdomere leading to degeneration of photoreceptors. Trp^P365 /+ also led to the up-regulation of CaMKII, which is beneficial as suppression of CaMKII accelerated retinal degeneration. We explored the regulation of TRP by investigating the genetic interaction between Trp^P365 /+ and mutants affecting the turnover of diacylglycerol (DAG). We show a loss of phospholipase C in norpA^P24 exhibited a great reduction of the DAG content delayed degeneration of Trp^P365 /+ photoreceptors. In contrast, knockdown or mutations in DAG lipase (InaE) that is accompanied by slightly reduced levels of most DAG but an increased level of DAG 34:1, exacerbated retinal degeneration of Trp^P365 /+. Together, our findings support the notion that DAG plays a role in regulating TRP. Interestingly, DAG lipase is likely required during photoreceptor development as Trp^P365 /+; inaE^N125 double mutants contained severely degenerated rhabdomeres.