Segmentation of Low-Light Optical Coherence Tomography Angiography Images under the Constraints of Vascular Network Topology.

Optical coherence tomography angiography (OCTA) offers critical insights into the retinal vascular system, yet its full potential is hindered by challenges in precise image segmentation. Current methodologies struggle with imaging artifacts and clarity issues, particularly under low-light conditions and when using various high-speed CMOS sensors. These challenges are particularly pronounced when diagnosing and classifying diseases such as branch vein occlusion (BVO). To address these issues, we have developed a novel network based on topological structure generation, which transitions from superficial to deep retinal layers to enhance OCTA segmentation accuracy. Our approach not only demonstrates improved performance through qualitative visual comparisons and quantitative metric analyses but also effectively mitigates artifacts caused by low-light OCTA, resulting in reduced noise and enhanced clarity of the images. Furthermore, our system introduces a structured methodology for classifying BVO diseases, bridging a critical gap in this field. The primary aim of these advancements is to elevate the quality of OCTA images and bolster the reliability of their segmentation. Initial evaluations suggest that our method holds promise for establishing robust, fine-grained standards in OCTA vascular segmentation and analysis.

A stripe rust fungal effector PstSIE1 targets TaSGT1 to facilitate pathogen infection.

Puccinia striiformis f. sp. tritici (Pst), the causal agent of stripe rust, is a destructive pathogen of Triticum aestivum (wheat), threatening wheat production worldwide. Pst delivers hundreds of effectors to manipulate processes in its hosts during infection. The SGT1 (suppressor of the G2 allele of skp1), RAR1 (required for Mla12 resistance) and HSP90 (heat-shock protein 90) proteins form a chaperone complex that acts as a core modulator in plant immunity. However, little is known about how Pst effectors target this immune component to suppress plant immunity. Here, we identified a Pst effector PstSIE1 that interacts with TaSGT1 in wheat and is upregulated during the early infection stage. Transient expression of PstSIE1 suppressed cell death in Nicotiana benthamiana induced by VmE02 and PcNLP2. Transgenic expression of PstSIE1-RNAi constructs in wheat significantly reduced the virulence of Pst. Overexpression of PstSIE1 in wheat increased the number of rust pustules and reduced the accumulation of reactive oxygen species (ROS), indicating that PstSIE1 functions as an important pathogenicity factor in Pst. PstSIE1 was found to compete with TaRAR1 to bind TaSGT1, thus disrupting the formation of the TaRAR1-TaSGT1 subcomplex. Taken together, PstSIE1 is an important Pst effector targeting the immune component TaSGT1 and involved in suppressing wheat defense.

TaClpS1, negatively regulates wheat resistance against Puccinia striiformis f. sp. tritici.

BACKGROUND: The degradation of intracellular proteins plays an essential role in plant responses to stressful environments. ClpS1 and E3 ubiquitin ligase function as adaptors for selecting target substrates in caseinolytic peptidase (Clp) proteases pathways and the 26S proteasome system, respectively. Currently, the role of E3 ubiquitin ligase in the plant immune response to pathogens is well defined. However, the role of ClpS1 in the plant immune response to pathogens remains unknown. RESULTS: Here, wheat (Triticum aestivum) ClpS1 (TaClpS1) was studied and resulted to encode 161 amino acids, containing a conserved ClpS domain and a chloroplast transit peptide (1-32 aa). TaClpS1 was found to be specifically localized in the chloroplast when expressed transiently in wheat protoplasts. The transcript level of TaClpS1 in wheat was significantly induced during infection by Puccinia striiformis f. sp. tritici (Pst). Knockdown of TaClpS1 via virus-induced gene silencing (VIGS) resulted in an increase in wheat resistance against Pst, accompanied by an increase in the hypersensitive response (HR), accumulation of reactive oxygen species (ROS) and expression of TaPR1 and TaPR2, and a reduction in the number of haustoria, length of infection hypha and infection area of Pst. Furthermore, heterologous expression of TaClpS1 in Nicotiana benthamiana enhanced the infection by Phytophthora parasitica. CONCLUSIONS: These results suggest that TaClpS1 negatively regulates the resistance of wheat to Pst.

A stripe rust effector Pst18363 targets and stabilises TaNUDX23 that promotes stripe rust disease.

Wheat stripe rust, caused by Puccinia striiformis f. sp. tritici (Pst), poses a tremendous threat to the production of wheat worldwide. The molecular mechanisms of Pst effectors that regulate wheat immunity are poorly understood. In this study, we identified an effector Pst18363 from Pst that suppresses plant cell death in Nicotiana benthamiana and in wheat. Knocking down Pst18363 expression by virus-mediated host-induced gene silencing significantly decreased the number of rust pustules, indicating that Pst18363 functions as an important pathogenicity factor in Pst. Pst18363 was proven to interact with wheat Nudix hydrolase 23 TaNUDX23. In wheat, silencing of TaNUDX23 by virus-induced gene silencing increased reactive oxygen species (ROS) accumulation induced by the avirulent Pst race CYR23, whereas overexpression of TaNUDX23 suppressed ROS accumulation induced by flg22 in Arabidopsis. In addition, TaNUDX23 suppressed Pst candidate effector Pst322-trigged cell death by decreasing ROS accumulation in N. benthamiana. Knocking down of TaNUDX23 expression attenuated Pst infection, indicating that TaNUDX23 is a negative regulator of defence. In N. benthamiana, Pst18363 stabilises TaNUDX23. Overall, our data suggest that Pst18363 stabilises TaNUDX23, which suppresses ROS accumulation to facilitate Pst infection.