Silencing of two insulin receptor genes disrupts nymph-adult transition of alate brown citrus aphid

Insulin receptors play key roles in growth, development, and polymorphism in insects. Here, we report two insulin receptor genes (AcInR1 and AcInR2) from the brown citrus aphid, Aphis (Toxoptera) citricidus. Transcriptional analyses showed that AcInR1 increased during the nymph-adult transition in alate aphids, while AcInR2 had the highest expression level in second instar nymphs. AcInR1 is important in aphid development from fourth instar nymphs to adults as verified by dsRNA feeding mediated RNAi. The silencing of AcInR1 or/and AcInR2 produced a variety of phenotypes including adults with normal wings, malformed wings, under-developed wings, and aphids failing to develop beyond the nymphal stages. Silencing of AcInR1 or AcInR2 alone, and co-silencing of both genes, resulted in 73% or 60%, and 87% of aphids with problems in the transition from nymph to normal adult. The co-silencing of AcInR1 and AcInR2 resulted in 62% dead nymphs, but no mortality occurred by silencing of AcInR1 or AcInR2 alone. Phenotypes of adults in the dsInR1 and dsInR2 were similar. The results demonstrate that AcInR1 and AcInR2 are essential for successful nymph-adult transition in alate aphids and show that RNAi methods may be useful for the management of this pest

Spectroscopy of q3qˉ3\rm{q}^3\bar{\rm{q}}^3-States in Quark Model and Baryon-Antibaryon Enhancements

We study the mass spectrum of the $\rm{q}^3\bar{\rm{q}}^3$ mesons both from the quark model with triquark correlations and from common quark model with colormagnetic interactions and with relative S-waves between quarks. Two cluster configurations $(\rm{q}^3)-(\bar{\rm{q}}^3)$ and $(\rm{q}^2\bar{\rm{q}})-(\rm{q}\bar{\rm{q}}^2)$ are considered. In the spectrum we find rather stable states which have the same quantum number with particle resonances which are corresponding to the $p\bar{p}$ enhancement, $p\bar{\Lambda}$ enhancement and $\Lambda\bar{\Lambda}$ enhancement with spin-$\mathbf{0}$ or $\mathbf{1}$. This imply these enhancements are NOT experimental artifacts. The color-spin-flavor structures of $p\bar{p}$, $p\bar{\Lambda}$, and $\Lambda\bar{\Lambda}$ enhancements are revealed. The existence of spin-$\mathbf{1}$ $\Lambda\bar{\Lambda}, p\bar{\Lambda}, p\bar{p}$ enhancements is predicted.Comment: 45 pages, 5 figure

Decentralized Federated Reinforcement Learning for User-Centric Dynamic TFDD Control

The explosive growth of dynamic and heterogeneous data traffic brings great challenges for 5G and beyond mobile networks. To enhance the network capacity and reliability, we propose a learning-based dynamic time-frequency division duplexing (D-TFDD) scheme that adaptively allocates the uplink and downlink time-frequency resources of base stations (BSs) to meet the asymmetric and heterogeneous traffic demands while alleviating the inter-cell interference. We formulate the problem as a decentralized partially observable Markov decision process (Dec-POMDP) that maximizes the long-term expected sum rate under the users' packet dropping ratio constraints. In order to jointly optimize the global resources in a decentralized manner, we propose a federated reinforcement learning (RL) algorithm named federated Wolpertinger deep deterministic policy gradient (FWDDPG) algorithm. The BSs decide their local time-frequency configurations through RL algorithms and achieve global training via exchanging local RL models with their neighbors under a decentralized federated learning framework. Specifically, to deal with the large-scale discrete action space of each BS, we adopt a DDPG-based algorithm to generate actions in a continuous space, and then utilize Wolpertinger policy to reduce the mapping errors from continuous action space back to discrete action space. Simulation results demonstrate the superiority of our proposed algorithm to benchmark algorithms with respect to system sum rate

Deacetylation of topoisomerase I is an important physiological function of E. coli CobB

Escherichia coli topoisomerase I (TopA), a regulator of global and local DNA supercoiling, is modified by Nε-Lysine acetylation. The NAD+-dependent protein deacetylase CobB can reverse both enzymatic and non-enzymatic lysine acetylation modification in E. coli. Here, we show that the absence of CobB in a ΔcobB mutant reduces intracellular TopA catalytic activity and increases negative DNA supercoiling. TopA expression level is elevated as topA transcription responds to the increased negative supercoiling. The slow growth phenotype of the ΔcobB mutant can be partially compensated by further increase of intracellular TopA level via overexpression of recombinant TopA. The relaxation activity of purified TopA is decreased by in vitro non-enzymatic acetyl phosphate mediated lysine acetylation, and the presence of purified CobB protects TopA from inactivation by such non-enzymatic acetylation. The specific activity of TopA expressed from His-tagged fusion construct in the chromosome is inversely proportional to the degree of in vivo lysine acetylation during growth transition and growth arrest. These findings demonstrate that E. coli TopA catalytic activity can be modulated by lysine acetylation-deacetylation, and prevention of TopA inactivation from excess lysine acetylation and consequent increase in negative DNA supercoiling is an important physiological function of the CobB protein deacetylase