Mutations in an Atypical TIR-NB-LRR-LIM Resistance Protein Confer Autoimmunity

In order to defend against microbial infection, plants employ a complex immune system that relies partly on resistance (R) proteins that initiate intricate signaling cascades upon pathogen detection. The resistance signaling network utilized by plants is only partially characterized. A genetic screen conducted to identify novel defense regulators involved in this network resulted in the isolation of the snc6-1D mutant. Positional cloning revealed that this mutant contained a molecular lesion in the chilling sensitive 3 (CHS3) gene, thus the allele was renamed chs3-2D. CHS3 encodes a TIR-NB-LRR R protein that contains a C-terminal zinc-binding LIM (Lin-11, Isl-1, Mec-3) domain. Although this protein has been previously implicated in cold stress and defense response, the role of the LIM domain in modulating protein activity is unclear. The chs3-2D allele contains a G to A point mutation causing a C1340 to Y1340 substitution close to the LIM domain. It encodes a dominant gain-of-function mutation. The chs3-2D mutant is severely stunted and displays curled leaf morphology. Additionally, it constitutively expresses PATHOGENESIS-RELATED (PR) genes, accumulates salicylic acid, and shows enhanced resistance to the virulent oomycete isolate Hyaloperonospora arabidopsidis (H.a.) Noco2. Subcellular localization assays using GFP fusion constructs indicate that both CHS3 and chs3-2D localize to the nucleus. A third chs3 mutant allele, chs3-3D, was identified in an unrelated genetic screen in our lab. This allele contains a C to T point mutation resulting in an M1017 to V1017 substitution in the LRR–LIM linker region. Additionally, a chs3-2D suppressor screen identified two revertant alleles containing secondary mutations that abolish the mutant morphology. Analysis of the locations of these molecular lesions provides support for the hypothesis that the LIM domain represses CHS3 R-like protein activity. This repression may occur through either autoinhibition or binding of a negative defense regulator

Impaired Magnesium Protoporphyrin IX Methyltransferase (ChlM) Impedes Chlorophyll Synthesis and Plant Growth in Rice

Magnesium protoporphyrin IX methyltransferase (ChlM) catalyzes the formation of magnesium protoporphyrin IX monomethylester (MgPME) from magnesium protoporphyrin IX (MgP) in the chlorophyll synthesis pathway. However, no ChlM gene has yet been identified and studied in monocotyledonous plants. In this study, a spontaneous mutant, yellow-green leaf 18 (ygl18), was isolated from rice (Oryza sativa). This mutant showed yellow-green leaves, decreased chlorophyll level, and climate-dependent growth differences. Map-based cloning of this mutant identified the YGL18 gene LOC_Os06g04150. YGL18 is expressed in green tissues, especially in leaf organs, where it functions in chloroplasts. YGL18 showed an amino-acid sequence similarity to that of ChlM from different photosynthetic organisms. In vitro enzymatic assays demonstrated that YGL18 performed ChlM enzymatic activity, but ygl18 had nearly lost all ChlM activity. Correspondingly, the substrate MgP was largely accumulated while the product MgPME was reduced in ygl18 leaves. YGL18 is required for light-dependent and photoperiod-regulated chlorophyll synthesis. The retarded growth of ygl18 mutant plants was caused by the high light intensity. Moreover, the higher light intensity and longer exposure in high light intensity even made the ygl18 plants be more susceptible to death. Based on these results, it is suggested that YGL18 plays essential roles in light-related chlorophyll synthesis and light intensity–involved plant growth

China's low-emission pathways toward climate-neutral livestock production for animal-derived foods

Funding Information: This research was supported by the National Natural Science Foundation of China (Grant No. 31922080 and 31872403 ), China Agriculture Research System of MOF and MARA and the Hunan province science and technology plan (Grant No. 2022NK2021 ).Peer reviewedPublisher PD

Global Analysis of UDP Glucose Pyrophosphorylase (UDPGP) Gene Family in Plants: Conserved Evolution Involved in Cell Death

UDP glucose pyrophosphorylase (UDPGP) family genes have been reported to play essential roles in cell death or individual survival. However, a systematic analysis on UDPGP gene family has not been performed yet. In this study, a total of 454 UDPGP proteins from 76 different species were analyzed. The analyses of the phylogenetic tree and orthogroups divided UDPGPs into three clades, including UDP-N-acetylglucosamine pyrophosphorylase (UAP), UDP-glucose pyrophosphorylase (UGP, containing UGP-A and UGP-B), and UDP-sugar pyrophosphorylase (USP). The evolutionary history of the UDPGPs indicated that the members of UAP, USP, and UGP-B were relatively conserved while varied in UGP-A. Homologous sequences of UGP-B and USP were found only in plants. The expression profile of UDPGP genes in Oryza sativa was mainly motivated under jasmonic acid (JA), abscisic acid (ABA), cadmium, and cold treatments, indicating that UDPGPs may play an important role in plant development and environment endurance. The key amino acids regulating the activity of UDPGPs were analyzed, and almost all of them were located in the NB-loop, SB-loop, or conserved motifs. Analysis of the natural variants of UDPGPs in rice revealed that only a few missense mutants existed in coding sequences (CDSs), and most of the resulting variations were located in the non-motif sites, indicating the conserved structure and function of UDPGPs in the evolution. Furthermore, alternative splicing may play a key role in regulating the activity of UDPGPs. The spatial structure prediction, enzymatic analysis, and transgenic verification of UAP isoforms illustrated that the loss of N- and C-terminal sequences did not affect the overall 3D structures, but the N- and C-terminal sequences are important for UAP genes to maintain their enzymatic activity. These results revealed a conserved UDPGP gene family and provided valuable information for further deep functional investigation of the UDPGP gene family in plants

A Logistic Regression Mixture Model for Interval Mapping of Genetic Trait Loci Affecting Binary Phenotypes

Often in genetic research, presence or absence of a disease is affected by not only the trait locus genotypes but also some covariates. The finite logistic regression mixture models and the methods under the models are developed for detection of a binary trait locus (BTL) through an interval-mapping procedure. The maximum-likelihood estimates (MLEs) of the logistic regression parameters are asymptotically unbiased. The null asymptotic distributions of the likelihood-ratio test (LRT) statistics for detection of a BTL are found to be given by the supremum of a χ(2)-process. The limiting null distributions are free of the null model parameters and are determined explicitly through only four (backcross case) or nine (intercross case) independent standard normal random variables. Therefore a threshold for detecting a BTL in a flanking marker interval can be approximated easily by using a Monte Carlo method. It is pointed out that use of a threshold incorrectly determined by reading off a χ(2)-probability table can result in an excessive false BTL detection rate much more severely than many researchers might anticipate. Simulation results show that the BTL detection procedures based on the thresholds determined by the limiting distributions perform quite well when the sample sizes are moderately large