Cell–cell communication and axis specification in the Drosophila oocyte

AbstractIntercellular communication between the somatic and germline cells is vital to development of the Drosophila egg chamber. One critical outcome of this communication is the polarization of the oocyte along the anterior–posterior axis, a process induced by an unknown signal from the somatic follicle cells to the oocyte. The existence of this signal has been inferred from several reports demonstrating that the differentiation and patterning of the follicle cells by the spatially restricted activation of certain cell-signaling pathways is necessary for axis formation in the oocyte. These reports have also provided a framework for understanding how these signaling pathways are integrated to generate the follicle-cell pattern, but the precise role of the follicle cells in anterior–posterior axis formation remains enigmatic. Research has identified several genes that appear to be involved in the polarizing communication from the follicle cells to the oocyte. Interestingly the proteins encoded by most of these genes are associated with the extracellular matrix, suggesting a pivotal role for this complex biological component in the polarizing communication between the follicle cells and the oocyte. This review summarizes the findings in this area, and uses the experimental analyses of these genes to evaluate various models describing the possible nature of the polarizing signal, and the role of these genes in it

Environment-Invariant Curriculum Relation Learning for Fine-Grained Scene Graph Generation

The scene graph generation (SGG) task is designed to identify the predicates based on the subject-object pairs.However,existing datasets generally include two imbalance cases: one is the class imbalance from the predicted predicates and another is the context imbalance from the given subject-object pairs, which presents significant challenges for SGG. Most existing methods focus on the imbalance of the predicted predicate while ignoring the imbalance of the subject-object pairs, which could not achieve satisfactory results. To address the two imbalance cases, we propose a novel Environment Invariant Curriculum Relation learning (EICR) method, which can be applied in a plug-and-play fashion to existing SGG methods. Concretely, to remove the imbalance of the subject-object pairs, we first construct different distribution environments for the subject-object pairs and learn a model invariant to the environment changes. Then, we construct a class-balanced curriculum learning strategy to balance the different environments to remove the predicate imbalance. Comprehensive experiments conducted on VG and GQA datasets demonstrate that our EICR framework can be taken as a general strategy for various SGG models, and achieve significant improvements.Comment: ICCV2023. arXiv admin note: text overlap with arXiv:2203.11654 by other author

Ras promotes cell survival by antagonizing both JNK and Hid signals in the Drosophila eye

<p>Abstract</p> <p>Background</p> <p>Programmed cell death, or apoptosis, is a fundamental physiological process during normal development or in pathological conditions. The activation of apoptosis can be elicited by numerous signalling pathways. Ras is known to mediate anti-apoptotic signals by inhibiting Hid activity in the <it>Drosophila </it>eye. Here we report the isolation of a new loss-of-function <it>ras </it>allele, <it>ras</it>^<it>KP</it>, which causes excessive apoptosis in the <it>Drosophila </it>eye.</p> <p>Results</p> <p>This new function is likely to be mediated through the JNK pathway since the inhibition of JNK signalling can significantly suppress <it>ras</it>^<it>KP</it>-induced apoptosis, whereas the removal of <it>hid </it>only weakly suppresses the phenotype. Furthermore, the reduction of JNK signalling together with the expression of the baculovirus caspase inhibitor p35, which blocks Hid activity, strongly suppresses the <it>ras</it>^{<it>KP </it>}cell death. In addition, we find a strong correlation between <it>ras</it>^<it>KP</it>-induced apoptosis in the eye disc and the activation of JNK signalling.</p> <p>Conclusion</p> <p>In the <it>Drosophila </it>eye, Ras may protect cells from apoptosis by inhibiting both JNK and Hid activities. Surprisingly, reducing Ras activity in the wing, however, does not cause apoptosis but rather affects cell and organ size. Thus, in addition to its requirement for cell viability, Ras appears to mediate different biological roles depending on the developmental context and on the level of its expression.</p

Regulation of the endocycle/gene amplification switch by Notch and ecdysone signaling

The developmental signals that regulate the switch from genome-wide DNA replication to site-specific amplification remain largely unknown. Drosophila melanogaster epithelial follicle cells, which begin synchronized chorion gene amplification after three rounds of endocycle, provide an excellent model for study of the endocycle/gene amplification (E/A) switch. Here, we report that down-regulation of Notch signaling and activation of ecdysone receptor (EcR) are required for the E/A switch in these cells. Extended Notch activity suppresses EcR activation and prevents exit from the endocycle. Tramtrack (Ttk), a zinc-finger protein essential for the switch, is regulated negatively by Notch and positively by EcR. Ttk overexpression stops endoreplication prematurely and alleviates the endocycle exit defect caused by extended Notch activity or removal of EcR function. Our results reveal a developmental pathway that includes down-regulation of Notch, activation of the EcR, up-regulation of Ttk to execute the E/A switch, and, for the first time, the genetic interaction between Notch and ecdysone signaling in regulation of cell cycle programs and differentiation