Identification of reference markers for characterizing honey bee (Apis mellifera) hemocyte classes

Cell mediated immunity of the honey bee (Apis mellifera) involves the activity of several hemocyte populations, currently defined by morphological features and lectin binding characteristics. The objective of the present study was to identify molecular markers capable of characterizing subsets of honey bee hemocytes. We developed and employed monoclonal antibodies with restricted reactions to functionally distinct hemocyte subpopulations. Melanizing cells, known as oenocytoids, were defined by an antibody to prophenoloxidase, aggregating cells were identified by the expression of Hemolectin, and phagocytic cells were identified by a marker expressed on granulocytes. We anticipate that this combination of antibodies not only allows for the detection of functionally distinct hemocyte subtypes, but will help to further the exploration of hematopoietic compartments, as well as reveal details of the honey bee cellular immune defense against parasites and microbes

GMAP is an Atg8a-interacting protein that regulates Golgi turnover In Drosophila

Selective autophagy receptors and adapters contain short linear motifs called LIR motifs (LC3-interacting region), which are required for the interaction with the Atg8-family proteins. LIR motifs bind to the hydrophobic pockets of the LIR motif docking site (LDS) of the respective Atg8-family proteins. The physiological significance of LDS docking sites has not been clarified in vivo. Here, we show that Atg8a-LDS mutant Drosophila flies accumulate autophagy substrates and have reduced lifespan. Using quantitative proteomics to identify the proteins that accumulate in Atg8a-LDS mutants, we identify the cis-Golgi protein GMAP (Golgi microtubule-associated protein) as a LIR motif-containing protein that interacts with Atg8a. GMAP LIR mutant flies exhibit accumulation of Golgi markers and elongated Golgi morphology. Our data suggest that GMAP mediates the turnover of Golgi by selective autophagy to regulate its morphology and size via its LIR motif-mediated interaction with Atg8a

In Search of Lost Bandwidth: Extensive Reordering of DRAM Accesses on FPGA

For efficient acceleration on FPGA, it is essential for external memory to match the throughput of the processing pipelines. However, the usable DRAM bandwidth decreases significantly if the access pattern causes frequent row conflicts. Memory controllers reorder DRAM commands to minimize row conflicts; however, general-purpose controllers must also minimize latency, which limits the depth of the internal queues over which reordering can occur. For latency-insensitive applications with irregular access pattern, nonblocking caches that support thousands of in-flight misses (miss-optimized memory systems) improve bandwidth utilization by reusing the same memory response to serve as many incoming requests as possible. However, they do not improve the irregularity of the access pattern sent to the memory, meaning that row conflicts will still be an issue. Sending out bursts instead of single memory requests makes the access pattern more sequential; however, realistic implementations trade high throughput for some unnecessary data in the bursts, leading to bandwidth wastage that cancels out part of the gains from regularization. In this paper, we present an alternative approach to extend the scope of DRAM row conflict minimization beyond the possibilities of general-purpose DRAM controllers. We use the thousands of future memory requests that spontaneously accumulate inside the miss-optimized memory system to implement an efficient large-scale reordering mechanism. By reordering single requests instead of sending bursts, we regularize the memory access pattern in a way that increases bandwidth utilization without incurring in any data wastage. Our solution outperforms the baseline miss-optimized memory system by up to 81% and has better worst, average, and best performance than DynaBurst across 15 benchmarks and 30 architectures

Eater cooperates with Multiplexin to drive the formation of hematopoietic compartments

Blood development in multicellular organisms relies on specific tissue microenvironments that nurture hematopoietic precursors and promote their self-renewal, proliferation, and differentiation. The mechanisms driving blood cell homing and their interactions with hematopoietic microenvironments remain poorly understood. Here, we use the Drosophila melanogaster model to reveal a pivotal role for basement membrane composition in the formation of hematopoietic compartments. We demonstrate that by modulating extracellular matrix components, the fly blood cells known as hemocytes can be relocated to tissue surfaces where they function similarly to their natural hematopoietic environment. We establish that the Collagen XV/XVIII ortholog Multiplexin in the tissue-basement membranes and the phagocytosis receptor Eater on the hemocytes physically interact and are necessary and sufficient to induce immune cell-tissue association. These results highlight the cooperation of Multiplexin and Eater as an integral part of a homing mechanism that specifies and maintains hematopoietic sites in Drosophil

Dynamic thermal management with proactive fan speed control through reinforcement learning

Dynamic Thermal Management (DTM) has become a major challenge since it directly affects Multiprocessors Systems-on-chip (MPSoCs) performance, power consumption, and reliability. In this work, we propose a transient fan model, enabling adaptive fan speed control simulation for efficient DTM. Our model is validated through a thermal test chip achieving less than 2°C error in the worst case. With multiple fan speeds, however, the DTM design space grows significantly, which can ultimately make conventional solutions impractical. We address this challenge through a reinforcement learning-based solution to proactively determine the number of active cores, operating frequency, and fan speed. The proposed solution is able to reduce fan power by up to 40% compared to a DTM with constant fan speed with less than 1% performance degradation. Also, compared to a state-of-the-art DTM technique our solution improves the performance by up to 19% for the same fan power

Dynamic Thermal Management with Proactive Fan Speed Control Through Reinforcement Learning

Dynamic Thermal Management (DTM) has become a major challenge since it directly affects Multiprocessors Systems-on-chip (MPSoCs) performance, power consumption, and reliability. In this work, we propose a transient fan model, enabling adaptive fan speed control simulation for efficient DTM. Our model is validated through a thermal test chip achieving less than 2°C error in the worst case. With multiple fan speeds, however, the DTM design space grows significantly, which can ultimately make conventional solutions impractical. We address this challenge through a reinforcement learning-based solution to proactively determine the number of active cores, operating frequency, and fan speed. The proposed solution is able to reduce fan power by up to 40% compared to a DTM with constant fan speed with less than 1% performance degradation. Also, compared to a state-of-the-art DTM technique our solution improves the performance by up to 19% for the same fan power

JNK-dependent cell cycle stalling in G2 promotes survival and senescence-like phenotypes in tissue stress

The restoration of homeostasis after tissue damage relies on proper spatial-temporal control of damage-induced apoptosis and compensatory proliferation. In Drosophila imaginal discs these processes are coordinated by the stress response pathway JNK. We demonstrate that JNK signaling induces a dose-dependent extension of G2 in tissue damage and tumors, resulting in either transient stalling or a prolonged but reversible cell cycle arrest. G2-stalling is mediated by downregulation of the G2/M-specific phosphatase String(Stg)/Cdc25. Ectopic expression of stg is sufficient to suppress G2-stalling and reveals roles for stalling in survival, proliferation and paracrine signaling. G2-stalling protects cells from JNK-induced apoptosis, but under chronic conditions, reduces proliferative potential of JNK-signaling cells while promoting non-autonomous proliferation. Thus, transient cell cycle stalling in G2 has key roles in wound healing but becomes detrimental upon chronic JNK overstimulation, with important implications for chronic wound healing pathologies or tumorigenic transformation

Dynamic Thermal Management with Proactive Fan Speed Control Through Reinforcement Learning

Dynamic Thermal Management (DTM) has become a major challenge since it directly affects Multiprocessors Systems-on-chip (MPSoCs) performance, power consumption, and reliability. In this work, we propose a transient fan model, enabling adaptive fan speed control simulation for efficient DTM. Our model is validated through a thermal test chip achieving less than 2◦ C error in the worst case. With multiple fan speeds, however, the DTM design space grows significantly, which can ultimately make conventional solutions impractical. We address this challenge through a reinforcement learning-based solution to proactively determine the number of active cores, operating frequency, and fan speed. The proposed solution is able to reduce fan power by up to 40% compared to a DTM with constant fan speed with less than 1% performance degradation. Also, compared to a state-of-the-art DTM technique our solution improves the performance by up to 19% for the same fan power

The raspberry Gene Is Involved in the Regulation of the Cellular Immune Response in Drosophila melanogaster

Drosophila is an extremely useful model organism for understanding how innate immune mechanisms defend against microbes and parasitoids. Large foreign objects trigger a potent cellular immune response in Drosophila larva. In the case of endoparasitoid wasp eggs, this response includes hemocyte proliferation, lamellocyte differentiation and eventual encapsulation of the egg. The encapsulation reaction involves the attachment and spreading of hemocytes around the egg, which requires cytoskeletal rearrangements, changes in adhesion properties and cell shape, as well as melanization of the capsule. Guanine nucleotide metabolism has an essential role in the regulation of pathways necessary for this encapsulation response. Here, we show that the Drosophila inosine 5'-monophosphate dehydrogenase (IMPDH), encoded by raspberry (ras), is centrally important for a proper cellular immune response against eggs from the parasitoid wasp Leptopilina boulardi. Notably, hemocyte attachment to the egg and subsequent melanization of the capsule are deficient in hypomorphic ras mutant larvae, which results in a compromised cellular immune response and increased survival of the parasitoid