MALT1 (mucosa-associated lymphoid tissue lymphoma translocation protein 1) serves as a pivotal mediator for NF-κB activation in response to a wide spectrum of transmembrane receptor stimuli. In the present study, a homolog of MALT1 is cloned from the Pacific white shrimp (Litopenaeus vannamei) named LvMALT1, and its potential function in shrimp innate immunity are explored. The open reading frame of LvMALT1 is 2364 bp that encodes 787 amino acids. The predicted LvMALT1 protein structure comprises a death domain, three immunoglobulin domains, and a caspase-like domain, exhibiting remarkable similarity to other homologs. LvMALT1 is a cytoplasmic-localized protein and could interact with LvTRAF6. Overexpression of LvMALT1 induces the activation of promoter elements governing the expression of several key antimicrobial peptides (AMPs), including Penaeidins (PENs) and Crustins (CRUs). Conversely, silencing of LvMALT1 leads to a reduction in the phosphorylation levels of Dorsal and Relish, along with a concomitant decline in the in vivo expression levels of multiple AMPs. Furthermore, LvMALT1 is prominently upregulated in response to a challenge by the white spot syndrome virus (WSSV), facilitating the NF-κB-mediated expression of AMPs as a defense against viral infection. Taken together, we identified a MALT1 homolog from shrimp L. vannamei, which plays a positive role in the TRAF6/NF-κB/AMPs axis mediated innate immunity.

In this paper, the deformation behavior of S32750 duplex stainless steel during low cycle fatigue was studied by controlling number of cycles. The microstructure of the specimens under different cycles was characterized by optical microscope (OM), scanning electron microscope (SEM), electron backscatter diffraction (EBSD) and transmission electron microscope (TEM). Microhardness of two phases was measured by a digital microhardness instrument. The results showed that the microhardness of ferrite increases significantly after the first 4000 cycles, while the austenite shows a higher strain hardening rate after fatigue fracture, and the microhardness of ferrite and austenite increases by 23 HV and 87 HV, respectively. Two-phase kernel average misorientation (KAM) diagram showed that the continuous accumulation of plastic deformation easily leads to the initiation of cracks inside the austenite and at the phase boundaries. The evolution of dislocation morphology in two phases was obviously different. With the increase of cycle number, the dislocation in ferrite gradually transforms from dislocation bundles and dislocation array to sub-grain structure, while the dislocation in austenite gradually develops from dipole array to ordered Taylor lattice network structure.