In this paper, we discuss the quantum circuit implementations of the lightweight authenticated encryption algorithm ASCON by using the NOT gates, CNOT gates, Toffoli gates, measurements, and the ...dynamic quantum circuits. Firstly, the quantum circuit of addition of constants is realized by adding the NOT gates according to the position of 1 in round constants. Secondly, the quantum circuit of S-box of the permutation is synthesized according to the classical circuit diagram of S-box. Then the linear layer functions are expressed in matrix form, and their quantum circuits are synthesized according to Gaussian elimination. Finally, we synthesize the whole quantum circuits according to the general diagrams of the authenticated encryption algorithm ASCON. The correctness of the quantum circuits of the S-box and the linear layer was verified by the Aer simulator of the IBM Quantum platform. As far as we know, this is the first implementation of the quantum circuits for the Authenticated Encryption with Associated Data (AEAD) of ASCON in-place. The maximum quantum resources for the three ASCON authenticated encryption algorithms were estimated. The quantum circuit of ASCON-128 uses a total of 320 qubits, 30,639 NOT gates, 128,814 CNOT gates, 8064 Toffoli gates, 10,752 measurements, and 5376 dynamic quantum circuits. The quantum circuit of ASCON-128a uses a total of 320 qubits, 23,558 NOT gates, 98,144 CNOT gates, 6144 Toffoli gates, 8192 measurements, and 4096 dynamic quantum circuits. The quantum circuit of ASCON-80pq uses a total of 320 qubits, 30,736 NOT gates, 128,814 CNOT gates, 8064 Toffoli gates, 10,752 measurements, and 5376 dynamic quantum circuits.
Investigations into the association between chicken traits and genetic variations provide helpful breeding information to improve production performance and economic benefits in chickens. The single ...nucleotide polymorphism technique is an important method in agricultural molecular breeding. In this study, we detected 11 SNPs in the CD36 gene, 2 SNPs (g.-1974 A>G, g.-1888 T>C) located in the 5′ flanking regions, 8 SNPs (g.23496 G>A, g.23643 C>T, g.23931 T>C, g.23937 G>A, g.31256 C>A, g.31258 C>T, g.31335 C>T, g.31534 A>C) located in the intron region, 1 SNPs (g.23743 G>T) located in the exon region and it belongs to synonymous mutation. In SNPs g.23743 G>T, the abdominal fat weight and abdominal fat weight rate of the GG genotype were lower than that of the TT genotype. In SNPs g.23931 T>C, the full-bore weight rate and half-bore weight rate of the TT genotype were higher compared with the CC genotype. And the SNPs g.-1888 T>C, g.23496 G>A, g.23643 C>T, g.31335 C>T and g.31534 A>C were significantly associated with skin yellowness traits, the cloacal skin yellowness before slaughter of the TT genotype was higher than that of the TC and CC genotype in SNPs g.-1888 T>C. Furthermore, 3 haplotypes of the above eleven SNPs were calculated and they correlated with heart weight, stomach weight, wing weight, leg skin yellowness and shin skin yellowness before slaughter. Finally, the CD36 expression profile displayed the expression pattern of CD36 mRNA variation in different tissues.
Prolactin (PRL) and growth hormone (GH) exhibit important roles in the immune system maintenance. In poultry, PRL mainly plays its roles in nesting, hatching, and reproduction, while GH is primarily ...responding to body weight, fat formation and feed conversion. In this review, we attempt to provide a critical overview of the relationship between PRL and GH, PRLR and GHR, and the immune response of poultry. We also propose a hypothesis that PRL, GH and their receptors might be used by viruses as viral receptors. This may provide new insights into the pathogenesis of viral infection and host immune response.
Skin color is an important economic trait in meat-type chickens. A uniform bright skin color can increase the sales value of chicken. Chickens with bright yellow skin are more popular in China, ...especially in the broiler market of South China. However, the skin color of chickens can vary because of differences in breeds, diet, health, and individual genetics. To obtain greater insight into the genetic factors associated with the process of skin pigmentation in chickens, we used a colorimeter and high-resolution skin photographs to measure and analyze the skin color of chickens. By analyzing 534 chickens of the same breed, age, and feed condition, we found that the yellowness values of the chickens varied within this population. A significant positive correlation was found between the cloacal skin yellowness values before and after slaughter, and the cloacal skin yellowness value of live chickens was positively correlated with the overall body skin yellowness value. Additionally, chicken skin yellowness exhibited low heritability, ranging from 0.07 to 0.27. Through RNA sequencing, 882 genes were found to be differentially expressed between the skin with the highest and lowest yellowness values. Some of these differentially expressed genes may play an important role in yellow pigment deposition in chicken skin, which included
, and
. In addition, we found that the expression and variations of the
gene, which is referred to as the yellow skin gene, cannot be used to estimate the skin yellowness value of chickens in this population. These data will help to further our understanding of chicken skin yellowness and might contribute to the selection of specific chicken strains with consistent skin coloration.
Background
Transmembrane proteins are vital for intercellular signalling and play important roles in the control of cell fate. However, their physiological functions and mechanisms of action in ...myogenesis and muscle disorders remain largely unexplored. It has been found that transmembrane protein 182 (TMEM182) is dramatically up‐regulated during myogenesis, but its detailed functions remain unclear. This study aimed to analyse the function of TMEM182 during myogenesis and muscle regeneration.
Methods
RNA sequencing, quantitative real‐time polymerase chain reaction, and immunofluorescence approaches were used to analyse TMEM182 expression during myoblast differentiation. A dual‐luciferase reporter assay was used to identify the promoter region of the TMEM182 gene, and a chromatin immunoprecipitation assay was used to investigate the regulation TMEM182 transcription by MyoD. We used chickens and TMEM182‐knockout mice as in vivo models to examine the function of TMEM182 in muscle growth and muscle regeneration. Chickens and mouse primary myoblasts were used to extend the findings to in vitro effects on myoblast differentiation and fusion. Co‐immunoprecipitation and mass spectrometry were used to identify the interaction between TMEM182 and integrin beta 1 (ITGB1). The molecular mechanism by which TMEM182 regulates myogenesis and muscle regeneration was examined by Transwell migration, cell wound healing, adhesion, glutathione‐S‐transferse pull down, protein purification, and RNA immunoprecipitation assays.
Results
TMEM182 was specifically expressed in skeletal muscle and adipose tissue and was regulated at the transcriptional level by the myogenic regulatory factor MyoD1. Functionally, TMEM182 inhibited myoblast differentiation and fusion. The in vivo studies indicated that TMEM182 induced muscle fibre atrophy and delayed muscle regeneration. TMEM182 knockout in mice led to significant increases in body weight, muscle mass, muscle fibre number, and muscle fibre diameter. Skeletal muscle regeneration was accelerated in TMEM182‐knockout mice. Furthermore, we revealed that the inhibitory roles of TMEM182 in skeletal muscle depend on ITGB1, an essential membrane receptor involved in cell adhesion and muscle formation. TMEM182 directly interacted with ITGB1, and this interaction required an extracellular hybrid domain of ITGB1 (aa 387–470) and a conserved region (aa 52–62) within the large extracellular loop of TMEM182. Mechanistically, TMEM182 modulated ITGB1 activation by coordinating the association between ITGB1 and laminin and regulating the intracellular signalling of ITGB1. Myogenic deletion of TMEM182 increased the binding activity of ITGB1 to laminin and induced the activation of the FAK‐ERK and FAK‐Akt signalling axes during myogenesis.
Conclusions
Our data reveal that TMEM182 is a novel negative regulator of myogenic differentiation and muscle regeneration.
Previous studies have demonstrated the role of N6-methyladenosine (m.sup.6A) RNA methylation in various biological processes, our research is the first to elucidate its specific impact on LCAT mRNA ...stability and adipogenesis in poultry. The 6 100-day-old female chickens were categorized into high (n = 3) and low-fat chickens (n = 3) based on their abdominal fat ratios, and their abdominal fat tissues were processed for MeRIP-seq and RNA-seq. An integrated analysis of MeRIP-seq and RNA-seq omics data revealed 16 differentially expressed genes associated with to differential m.sup.6A modifications. Among them, ELOVL fatty acid elongase 2 (ELOVL2), pyruvate dehydrogenase kinase 4 (PDK4), fatty acid binding protein 9 (PMP2), fatty acid binding protein 1 (FABP1), lysosomal associated membrane protein 3 (LAMP3), lecithin-cholesterol acyltransferase (LCAT) and solute carrier family 2 member 1 (SLC2A1) have ever been reported to be associated with adipogenesis. Interestingly, LCAT was down-regulated and expressed along with decreased levels of mRNA methylation methylation in the low-fat group. Mechanistically, the highly expressed ALKBH5 gene regulates LCAT RNA demethylation and affects LCAT mRNA stability. In addition, LCAT inhibits preadipocyte proliferation and promotes preadipocyte differentiation, and plays a key role in adipogenesis. In conclusion, ALKBH5 mediates RNA stability of LCAT through demethylation and affects chicken adipogenesis. This study provides a theoretical basis for further understanding of RNA methylation regulation in chicken adipogenesis.
Excessive abdominal fat deposition is an issue with general concern in broiler production, especially for Chinese native chicken breeds. A high-fat diet (HFD) can induce body weight gained and ...excessive fat deposition, and genes and pathways participate in fat metabolism and adipogenesis would be influenced by HFD. In order to reveal the main genes and pathways involved in chicken abdominal fat deposition, we used HFD and normal diet (ND) to feed a Chinese native chicken breed, respectively. Results showed that HFD can increase abdominal fat deposition and induce adipocyte hypertrophy. Additionally, we used RNA-sequencing to identify the differentially expressed genes (DEGs) between HFD and ND chickens in liver and abdominal fat. By analyzed these DEGs, we found that the many DEGs were enriched in fat metabolism related pathways, such as peroxisome proliferator-activated receptor (PPAR) signaling, fat digestion and absorption, extracellular matrix (ECM)-receptor interaction, and steroid hormone biosynthesis. Notably, the expression of
, which is a binding protein of
mRNA, was found to be induced in liver and abdominal fat by HFD. Ectopic expression of
in chicken liver-related cell line Leghorn strain M chicken hepatoma (LMH) cell revealed that
can regulate the expression of genes associated with fatty acid metabolism. In chicken preadipocytes (ICP cell line), we found that
can promote adipocyte proliferation and differentiation, and the lipid droplet content would be increased by overexpression of
. Taken together, this study provides new insights into understanding the genes and pathways involved in abdominal fat deposition of Chinese native broiler, and
is an important candidate gene for the study of fat metabolism and adipogenesis in chicken.
Adipose tissue is an important endocrine and energy-storage organ in organisms, and it plays a crucial role in the energy-metabolism balance. Previous studies have found that sex-linked dwarf (SLD) ...chickens generally have excessively high abdominal fat deposition during the growing period, which increases feeding costs. However, the underlying mechanism of this fat deposition during the growth of SLD chickens remains unknown.
The Oil Red O staining showed that the lipid-droplet area of SLD chickens was larger than that of normal chickens in E15 and 14d. Consistently, TG content in the livers of SLD chickens was higher than that of normal chickens in E15 and 14d. Further, lower ΔΨm and lower ATP levels and higher MDA levels were observed in SLD chickens than normal chickens in both E15 and 14d. We also found that overexpression of GHR reduced the expression of genes related to lipid metabolism (AMPK, PGC1α, PPARγ, FAS, C/EBP) and oxidative phosphorylation (CYTB, CYTC, COX1, ATP), as well as reducing ΔΨm and ATP levels and increasing MDA levels. In addition, overexpression of GHR inhibited fat deposition in CPPAs, as measured by Oil Red O staining. On the contrary, knockdown of GHR had the opposite effects in vitro.
In summary, we demonstrate that GHR promotes mitochondrial function and inhibits lipid peroxidation as well as fat deposition in vivo and in vitro. Therefore, GHR is essential for maintaining the stability of lipid metabolism and regulating mitochondrial function in chicken.
MicroRNAs (miRNAs) play a critical role in various biological processes through regulation of gene expression post-transcriptionally. Although miRNAs are involved in cell proliferation and ...differentiation in mammals, few reports regarding the effects of host miRNAs on macrophage activation and differentiation are available in birds. Here, we reported that gga-miR-200b-3p acts as a positive regulator, enhancing macrophage activation and differentiation using an avian model. We found that ectopic expression of gga-miR-200b-3p in HD11 cells enhances the amount of MHC-II-positive cells and promotes the expression of pro-inflammatory cytokines and that gga-miR-200b-3p directly targets monocyte to macrophage differentiation-associated (MMD). The inhibition of MMD by gga-miR-200b-3p enhances the activation and differentiation of HD11 cells and increases the expression of pro-inflammatory cytokines. Collectively, these findings highlight a crucial role of gga-miR-200b-3p in macrophage activation and differentiation in birds.
We propose a non-transversal but pieceable fault tolerant conversion circuit that is used to convert encoded information between five-qubit code and seven-qubit CSS code. Since a syndrome extraction ...circuit requiring fewer ancillary qubit resources would facilitate the realization of large-scale quantum computations, we further adapt a flag-assisted fault tolerant syndrome measurement scheme to reduce the cost of ancillary preparation. Numerical simulations are also performed to further analyze the performance of our conversion method.
PDF
