Effectiveness of a family empowerment program on caregiving capacity and adverse mood in caregivers of children with acute leukemia: a quasi-experimental study.

BACKGROUND: Family-centered empowerment programs have been widely used in the pediatric field. Therefore, the current study investigated the effectiveness of family empowerment programs on caregiving ability and adverse mood among caregivers of children with acute leukemia. OBJECTIVE: To evaluate the effect of a family empowerment program on the caregiving ability and adverse mood of caregivers of children with acute leukemia. METHODS: Sixty-eight children with acute leukemia and their family caregivers admitted to our hospital were selected for the study. The control group received routine care during hospitalization, and the family empowerment program was implemented in the intervention group to compare the changes in caregiving capacity (FCTI), illness uncertainty (PPUS) and anxiety(SAS)of the caregivers of the two groups. RESULTS: After 8 weeks of intervention, the FCTI score of the intervention group was significantly lower than that of the control group (P < 0.001), and the difference between the scores before and after the intervention was statistically significant (P < 0.001); the PPUS score of the intervention group was significantly lower than that of the control group (P < 0.05), and the difference between the scores before and after the intervention was statistically significant (P < 0.001); the SAS score of the intervention group was lower than that of the control group after intervention(P < 0.05), and the score difference before and after intervention was statistically significant (P < 0.001). CONCLUSION: Family empowerment program is beneficial in improving caregiving capacity and reducing disease uncertainty and anxiety among caregivers of children with acute leukemia. TRIAL REGISTRATION: Chinese Clinical Trial Registry ChiCTR2300073476 2023-07-12 Retrospectively registered.

PREMATURE SENESCENCE LEAF 50 Promotes Heat Stress Tolerance in Rice (Oryza sativa L.).

BACKGROUND: Heat stress is a major environmental factor that could induce premature leaf senescence in plants. So far, a few rice premature senescent leaf mutants have been reported to involve in heat tolerance. FINDINGS: We identified a premature senescence leaf 50 (psl50) mutant that exhibited a higher heat susceptibility with decreased survival rate, over-accumulated hydrogen peroxide (H2O2) content and increased cell death under heat stress compared with the wild-type. The causal gene PREMATURE SENESCENCE LEAF 50 (PSL50) was isolated by using initial map-based resequencing (IMBR) approach, and we found that PSL50 promoted heat tolerance probably by acting as a modulator of H2O2 signaling in response to heat stress in rice (Oryza sativa L.). CONCLUSIONS: PSL50 negatively regulates heat-induced premature leaf senescence in rice.

OsNAC109 regulates senescence, growth and development by altering the expression of senescence- and phytohormone-associated genes in rice.

KEY MESSAGE: We demonstrate that OsNAC109 regulates senescence, growth and development via binding to the cis-element CNTCSSNNSCAVG and altering the expression of multiple senescence- and hormone-associated genes in rice. The NAC family is one of the largest transcripton factor families in plants and plays an essential role in plant development, leaf senescence and responses to biotic/abiotic stresses through modulating the expression of numerous genes. Here, we isolated and characterized a novel yellow leaf 3 (yl3) mutant exhibiting arrested-growth, increased accumulation of reactive oxygen species (ROS), decreased level of soluble proteins, increased level of malondialdehyde (MDA), reduced activities of ROS scavenging enzymes, altered expression of photosynthesis and senescence/hormone-associated genes. The yellow leaf and arrested-growth trait was controlled by a single recessive gene located to chromosome 9. A single nucleotide substitution was detected in the mutant allele leading to premature termination of its coding protein. Genetic complementation could rescue the mutant phenotype while the YL3 knockout lines displayed similar phenotype to WT. YL3 was expressed in all tissues tested and predicted to encode a transcriptional factor OsNAC109 which localizes to the nucleus. It was confirmed that OsNAC109 could directly regulate the expression of OsNAP, OsNYC3, OsEATB, OsAMTR1, OsZFP185, OsMPS and OsGA2ox3 by targeting to the highly conserved cis-element CNTCSSNNSCAVG except OsSAMS1. Our results demonstrated that OsNAC109 is essential to rice leaf senescence, growth and development through regulating the expression of senescence- and phytohormone-associated genes in rice.

Characterization of a novel allele encoding pheophorbide a oxygenase in rice.

We identified a rapid cell death 2 (rcd2) mutant from an indica cultivar Zhongjian100 mutant bank. The red-brown lesions appeared firstly on young seedling leaves, then gradually merged and the leaves completely withered at the late tillering stage. rcd2 displayed apparent cell death at/around the lesions, accumulation of superoxide anion (O2-) and disturbed ROS scavenging system, impaired photosynthetic capacity with significantly reduced chlorophyll content. The lesion formation was controlled by a single recessive nuclear gene and induced by natural light as well as mechanical wounding. A single base mutation (A1726T) at the 6th exon of OsMH_03G0040800 resulted in I576F substitution in the encoding protein, pheophorbide a oxygenase (PAO). Functional complementation could rescue the mutant phenotype and PAO-knockout lines exhibited the similar phenotype to rcd2. The activity of PAO decreased significantly while the content of PAO substrate, pheophorbide a, increased apparently in rcd2. The expression of chlorophyll synthesis/degradation-related genes and the contents of metabolic intermediates were largely changed. Furthermore, the level of chlorophyllide a, the product of chlorophyllase, increased significantly, indicating chlorophyllase might play a role in chlorophyll degradation in rice. Our results suggested that the I576F substitution disrupted PAO function, leading to O2- accumulation and chlorophyll degradation breakdown in rice.

Chloroplast SRP54s are Essential for Chloroplast Development in Rice.

BACKGROUND: The chloroplast signal recognition particle 54 (cpSRP54) is known for targeting the light-harvesting complex proteins to thylakoids and plays a critical role for chloroplast development in Arabidopsis, but little is known in rice. Here, we reported two homologous cpSRP54s that affect chloroplast development and plant survival in rice. RESULTS: Two rice cpSRP54 homologues, OscpSRP54a and OscpSRP54b, were identified in present study. The defective OscpSRP54a (LOC_Os11g05552) was responsible for the pale green leaf phenotype of the viable pale green leaf 14 (pgl14) mutant. A single nucleotide substitution from G to A at the position 278, the first intron splicing site, was detected in LOC_Os11g05552 in pgl14. The wild type allele could rescue the mutant phenotype. Knockout lines of OscpSRP54b (LOC_Os11g05556) exhibited similar pale green phenotype to pgl14 with reduced chlorophyll contents and impaired chloroplast development, but showed apparently arrested-growth and died within 3 weeks. Both OscpSRP54a and OscpSRP54b were constitutively expressed mainly in shoots and leaves at the vegetative growth stage. Subcellular location indicated that both OscpSRP54a and OscpSRP54b were chloroplast-localized. Both OscpSRP54a and OscpSRP54b were able to interact with OscpSRP43, respectively. The transcript level of OscpSRP43 was significantly reduced while the transcript level of OscpSRP54b was apparently increased in pgl14. In contrast, the transcript levels of OscpSRP54a, OscpSRP43 and OscpSRP54b were all significantly decreased in OscpSRP54b knockout lines. CONCLUSION: Our study demonstrated that both OscpSRP54a and OscpSRP54b were essential for normal chloroplast development by interacting with OscpSRP43 in rice. OscpSRP54a and OscpSRP54b might play distinct roles in transporting different chloroplast proteins into thylakoids through cpSRP-mediated pathway.

The OsABCI7 Transporter Interacts with OsHCF222 to Stabilize the Thylakoid Membrane in Rice.

The thylakoid membrane is a highly complex membrane system in plants and plays crucial roles in the biogenesis of the photosynthetic apparatus and plant development. However, the genetic factors involved in chloroplast development and its relationship with intracellular metabolites are largely unknown. Here, a rice (Oryza sativa) chlorotic and necrotic leaf1 (cnl1) mutant was identified and map-based cloning revealed that a single base substitution followed by a 6-bp deletion in the ATP-binding cassette transporter I family member7 (OsABCI7) resulted in chlorotic and necrotic leaves with thylakoid membrane degradation, chlorophyll breakdown, photosynthesis impairment, and cell death in cnl1 Furthermore, the expression of OsABCI7 was inducible under lower temperatures, which severely affected cnl1 chloroplast development, and etiolated cnl1 seedlings were unable to recover to a normal green state under light conditions. Functional complementation and overexpression showed that OsABCI7 could rescue the cnl1 chlorotic and necrotic phenotype. OsABCI7 interacted with HIGH CHLOROPHYLL FLUORESCENCE222 (OsHCF222) to regulate cellular reactive oxygen species (ROS) homeostasis for thylakoid membrane stability. OsABCI7 localized to thylakoid membranes, while OsHCF222 targeted to endoplasmic reticulum and chloroplasts. Exogenous application of ascorbic acid eased the yellowish leaf phenotype by increasing chlorophyll content and alleviating ROS stress in cnl1 Unlike cnl1, the CRISPR/Cas9-mediated OsHCF222 knockout lines showed chlorotic leaves but were seedling lethal. Our results provide insight into the functions of ABC transporters in rice, especially within the relationship between ROS homeostasis and stability of thylakoid membranes.

Genetic and Physio-Biochemical Characterization of a Novel Premature Senescence Leaf Mutant in Rice (Oryza sativa L.).

Premature senescence greatly affects the yield production and the grain quality in plants, although the molecular mechanisms are largely unknown. Here, we identified a novel rice premature senescence leaf 85 (psl85) mutant from ethyl methane sulfonate (EMS) mutagenesis of cultivar Zhongjian100 (the wild-type, WT). The psl85 mutant presented a distinct dwarfism and premature senescence leaf phenotype, starting from the seedling stage to the mature stage, with decreasing level of chlorophyll and degradation of chloroplast, declined photosynthetic capacity, increased content of malonaldehyde (MDA), upregulated expression of senescence-associated genes, and disrupted reactive oxygen species (ROS) scavenging system. Moreover, endogenous abscisic acid (ABA) level was significantly increased in psl85 at the late aging phase, and the detached leaves of psl85 showed more rapid chlorophyll deterioration than that of WT under ABA treatment, indicating that PSL85 was involved in ABA-induced leaf senescence. Genetic analysis revealed that the premature senescence leaf phenotype was controlled by a single recessive nuclear gene which was finally mapped in a 47 kb region on the short arm of chromosome 7, covering eight candidate open reading frames (ORFs). No similar genes controlling a premature senescence leaf phenotype have been identified in the region, and cloning and functional analysis of the gene is currently underway.

Identification and Comparative Analysis of Premature Senescence Leaf Mutants in Rice (Oryza sativa L.).

Premature leaf senescence negatively impacts the grain yield in the important monocot rice (Oryza sativa L.); to understand the molecular mechanism we carried out a screen for mutants with premature senescence leaves in a mutant bank generated by ethyl methane sulfonate (EMS) mutagenesis of elite indica rice ZhongJian100. Five premature senescence leaf (psl15, psl50, psl89, psl117 and psl270) mutants were identified with distinct yellowish phenotypes on leaves starting from the tillering stage to final maturation. Moreover, these mutants exhibited significantly increased malonaldehyde content, decreased chlorophyll content, reduced numbers of chloroplast and grana thylakoid, altered photosynthetic ability and expression of photosynthesis-related genes. Furthermore, the expression of senescence-related indicator OsI57 was significantly up-regulated in four mutants. Histochemical analysis indicated that cell death and reactive oxygen species (ROS) accumulation occurred in the mutants with altered activities of ROS scavenging enzymes. Both darkness and abscisic acid (ABA) treatments could induce leaf senescence and resulted in up- or down-regulation of ABA metabolism-related genes in the mutants. Genetic analysis indicated that all the premature senescence leaf mutants were controlled by single non-allelic recessive genes. The data suggested that mechanisms underlying premature leaf senescence are likely different among the mutants. The present study would facilitate us to further fine mapping, cloning and functional characterization of the corresponding genes mediating the premature leaf senescence in rice.