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Background MicroRNAs (miRNAs) play essential regulatory roles in magnesium (Mg) imbalance by targeting key defense genes for cleavage or translational repression. miRNA targets in response to Mg deficiency and toxicity remain uncharacterized in mulberry ( Morus alba ) in Mg-induced stress. We, for the first time, investigated Mg-stress-responsive miRNAs and their targets in mulberry leaves using transcriptome-wide sequencing to identify miRNAs putatively involved in Mg-stress tolerance. In this study, Mg (MgSO 4 ) treatment applied in six concentration ranging from 0 mM/L (T0) as Mg deficiency, 1 mM/L and 2 mM/L (T1 and T2) as low Mg, 3 mM/L as the sufficiency or control (CK), and 6 mM/L and 9 mM/L (T6 and T9) as Mg excess for 20 days under controlled environment. Results Our analysis of differentially expressed miRNAs (DE-miRNAs) revealed that 254 out of the 893 miRNAs expressed across all samples showed differential expression, representing 28.44%. The study further identified 64 known miRNAs and 190 novel miRNAs within this set of differentially expressed miRNAs. These DE-miRNAs targeted a total of 39 Mg-induced genes and were predominantly involved in porphyrin, polyphenol oxidase, and phenylalanine ammonia-lyase metabolisms. For instance, miR477-x with ─25.1 minimum folding free energy and a minimum free energy ratio of 67.11% targeted four PAL genes, whereas novel miRNA (novel-m0001-5p) targeted eight genes in the polyphenol oxidase gene family involved in tyrosine metabolism. Additionally, four genes, including red chlorophyll catabolite reductase and uroporphyrinogen-III synthase, were targeted by miR529-x under Mg-induced treatments. Conclusion These findings enhance our understanding of plant miRNA function under nutrient stress and provide a foundation for improving mulberry Mg tolerance.

Background Viral diseases of sweet potatoes are causing severe crop losses worldwide. More than 30 viruses have been identified to infect sweet potatoes among which the sweet potato latent virus (SPLV), sweet potato mild speckling virus (SPMSV), sweet potato virus G (SPVG) and sweet potato virus 2 (SPV2) have been recognized as distinct species of the genus Potyvirus in the family Potyviridae . The sweet potato virus 2 (SPV2) is a primary pathogen affecting sweet potato crops. Methods In this study, we detected an SPV2 isolate (named SPV2-LN) in Ipomoea nil in China. The complete genomic sequence of SPV2 - LN was obtained using sequencing of small RNAs, RT - PCR, and RACE amplification. The codon usage, phylogeny, recombination analysis and selective pressure analysis were assessed on the SPV2 - LN genome. Results The complete genome of SPV2-LN consisted of 10,606 nt (GenBank No. OR842902), encoding 3425 amino acids. There were 28 codons in the SPV2-LN genome with a relative synonymous codon usage (RSCU) value greater than 1, of which 21 end in A/U. Among the 12 proteins of SPV2, P3 and P3N-PIPO exhibited the highest variability in their amino acid sequences, while P1 was the most conserved, with an amino acid sequence identity of 87 - 95.3%. The phylogenetic analysis showed that 21 SPV2 isolates were clustered into four groups, and SPV2 - LN was clustered together with isolate yu-17-47 (MK778808) in group IV. Recombination analysis indicated no major recombination sites in SPV2-LN. Selective pressure analysis showed d N / d S of the 12 proteins of SPV2 were less than 1, indicating that all were undergoing negative selection, except for P1N-PISPO. Conclusion This study identified a sweet potato virus, SPV2-LN, in Ipomoea nil. Sequence identities and genome analysis showed high similarity between our isolate and a Chinese isolate, yu-17-47, isolated from sweet potato. These results will provide a theoretical basis for understanding the genetic evolution and viral spread of SPV2.

Tomato cultivars containing the Tm‐22 resistance gene have been widely known to resist tobacco mosaic virus (TMV) and tomato mosaic virus. Tomato brown rugose fruit virus (ToBRFV), a new emerging tobamovirus, can infect tomato plants carrying the Tm‐22 gene. However, the virulence determinant of ToBRFV that overcomes the resistance conferred by the Tm‐22 gene remains unclear. In this study, we substituted the movement protein (MP) encoding sequences between ToBRFV and TMV infectious clones and conducted infectivity assays. The results showed that MP was the virulence determinant for ToBRFV to infect Tm‐22 transgenic Nicotiana benthamiana plants and Tm‐22‐carrying tomato plants. A TMV MP chimera with amino acid residues 60–186 of ToBRFV MP failed to induce hypersensitive cell death in the leaves of Tm‐22 transgenic N. benthamiana plants. Chimeric TMV containing residues 60–186 of ToBRFV MP could, but chimeric ToBRFV containing 61–187 residues of TMV MP failed to infect Tm‐22 transgenic N. benthamiana plants, indicating that 60–186 residues of MP were important for ToBRFV to overcome Tm‐22 gene‐mediated resistance. Further analysis showed that six amino acid residues, H67, N125, K129, A134, I147, and I168 of ToBRFV MP, were critical in overcoming Tm‐22‐mediated resistance in transgenic N. benthamiana plants and tomato plants. These results increase our understanding of the mechanism by which ToBRFV overcomes Tm‐22‐mediated resistance. Six amino acid residues, H67, N125, K129, A134, I147, and I168, located in the central region of the movement protein are involved in tomato brown rugose fruit virus to evade Tm‐22‐mediated resistance.

Tomato mottle mosaic virus (ToMMV) poses a threat to production and quality of tomato fruits. The Tm-2 2 gene confers resistance to some tobamoviruses by recognizing viral movement proteins. However, Tm-2 2 -mediated resistance against ToMMV is not well known. Here, we found that ToMMV could infect wild-type but not Tm-2 2 transgenic Nicotiana benthamiana plants and could also infect tomato cultivar Moneymaker but not resistant cultivar Jili with homozygous Tm-2 2 . Chimeric viral ToMMV ToBRFV−MP with swapped ToMMV MP to MP of tomato brown rugose fruit virus could systemically infect Tm-2 2 transgenic N. benthamiana and tomato cultivars Jili plants. Further, transient expression of ToMMV MP in the leaves of Tm-2 2 transgenic N. benthamiana plants induced hypersensitive response-associated cell death, suggesting that the MP of ToMMV was the avirulent factor for the Tm-2 2 resistance gene. ToMMV could infect Tm-2 2 -containing cultivar Jinpeng 1 but not Chaobei. Sequence analysis revealed that cultivars Chaobei and Jinpeng 1 were heterozygous, where Chaobei consists of Tm-2 2 and Tm-2 genes, while Jinpeng 1 consists of Tm-2 2 and tm-2 genes. Transient co-expression assays showed that both Tm-2 2 and Tm-2 but not tm-2 could recognize ToMMV MP and induce hypersensitivity response-associated cell death in N. benthamiana leaves, suggesting that homozygous tomato harboring Tm-2 2 and heterozygous tomato containing Tm-2 2 and Tm-2 may exhibit more durable resistance to ToMMV than heterozygous tomato carrying Tm-2 2 and tm-2 . Further, Tm-2 2 transgenic N. benthamiana and tomato cultivar Jili plants with silenced Tm-2 2 gene were susceptible to ToMMV. Also, silencing type-I J-domain MIP1 gene compromised Tm-2 2 -mediated resistance to ToMMV in Tm-2 2 transgenic N. benthamiana and tomato cultivar Jili. Moreover, we found that viral RNA could accumulate in the systemic leaves of Tm-2 2 transgenic N. benthamiana plants and tomato cultivar Jili at 35°C, but not at 20, 25, or 30°C. Altogether, our findings reveal that the Tm-2 2 confers resistance to ToMMV by recognizing MP, and the resistance is regulated by the allele combinations, accumulation levels of Tm-2 2 , MIP1 , and the temperature.

Tomato cultivars containing the Tm‐2 2 resistance gene have been widely known to resist tobacco mosaic virus (TMV) and tomato mosaic virus. Tomato brown rugose fruit virus (ToBRFV), a new emerging tobamovirus, can infect tomato plants carrying the Tm‐2 2 gene. However, the virulence determinant of ToBRFV that overcomes the resistance conferred by the Tm‐2 2 gene remains unclear. In this study, we substituted the movement protein (MP) encoding sequences between ToBRFV and TMV infectious clones and conducted infectivity assays. The results showed that MP was the virulence determinant for ToBRFV to infect Tm‐2 2 transgenic Nicotiana benthamiana plants and Tm‐2 2 ‐carrying tomato plants. A TMV MP chimera with amino acid residues 60–186 of ToBRFV MP failed to induce hypersensitive cell death in the leaves of Tm‐2 2 transgenic N. benthamiana plants. Chimeric TMV containing residues 60–186 of ToBRFV MP could, but chimeric ToBRFV containing 61–187 residues of TMV MP failed to infect Tm‐2 2 transgenic N. benthamiana plants, indicating that 60–186 residues of MP were important for ToBRFV to overcome Tm‐2 2 gene‐mediated resistance. Further analysis showed that six amino acid residues, H 67 , N 125 , K 129 , A 134 , I 147 , and I 168 of ToBRFV MP, were critical in overcoming Tm‐2 2 ‐mediated resistance in transgenic N. benthamiana plants and tomato plants. These results increase our understanding of the mechanism by which ToBRFV overcomes Tm‐2 2 ‐mediated resistance.

Abstract Tomato mottle mosaic virus (ToMMV) poses a threat to production and quality of tomato fruits. The Tm-2 2 gene confers resistance to some tobamoviruses by recognizing viral movement proteins. However, Tm-2 2 -mediated resistance against ToMMV is not well known. Here, we found that ToMMV could infect wild-type but not Tm-2 2 transgenic Nicotiana benthamiana plants and could also infect tomato cultivar Moneymaker but not resistant cultivar Jili with homozygous Tm-2 2 . Chimeric viral ToMMVToBRFV−MP with swapped ToMMV MP to MP of tomato brown rugose fruit virus could systemically infect Tm-2 2 transgenic N. benthamiana and tomato cultivars Jili plants. Further, transient expression of ToMMV MP in the leaves of Tm-2 2 transgenic N. benthamiana plants induced hypersensitive response-associated cell death, suggesting that the MP of ToMMV was the avirulent factor for the Tm-2 2 resistance gene. ToMMV could infect Tm-2 2 -containing cultivar Jinpeng 1 but not Chaobei. Sequence analysis revealed that cultivars Chaobei and Jinpeng 1 were heterozygous, where Chaobei consists of Tm-2 2 and Tm-2 genes, while Jinpeng 1 consists of Tm-2 2 and tm-2 genes. Transient co-expression assays showed that both Tm-2 2 and Tm-2 but not tm-2 could recognize ToMMV MP and induce hypersensitivity response-associated cell death in N. benthamiana leaves, suggesting that homozygous tomato harboring Tm-2 2 and heterozygous tomato containing Tm-2 2 and Tm-2 may exhibit more durable resistance to ToMMV than heterozygous tomato carrying Tm-2 2 and tm-2. Further, Tm-2 2 transgenic N. benthamiana and tomato cultivar Jili plants with silenced Tm-2 2 gene were susceptible to ToMMV. Also, silencing type-I J-domain MIP1 gene compromised Tm-2 2 -mediated resistance to ToMMV in Tm-2 2 transgenic N. benthamiana and tomato cultivar Jili. Moreover, we found that viral RNA could accumulate in the systemic leaves of Tm-2 2 transgenic N. benthamiana plants and tomato cultivar Jili at 35°C, but not at 20, 25, or 30°C. Altogether, our findings reveal that the Tm-2 2 confers resistance to ToMMV by recognizing MP, and the resistance is regulated by the allele combinations, accumulation levels of Tm-2 2 , MIP1, and the temperature.

To the Editor: Wanzer and colleagues' thorough review of the physician's responsibility toward dying patients (March 30 issue) 1 could have been even more helpful in two ways. First, it could have explicitly acknowledged that it is not chiefly the technical aspects of caring for the dying patient that \"tax the ingenuity and equanimity of the most skilled health professionals.\" Rather, it is the existential aspects, because they impinge on the physician as a person, not just as a professional in a social role. The white-coated professional technician is challenged to formulate prognoses with sometimes ambiguous data, to adjust constantly the . . . No extract is available for articles shorter than 400 words.