The fragile X mental retardation protein (FMRP) is a selective RNA-binding protein implicated in regulating translation of its mRNA ligands. The absence of FMRP results in fragile X syndrome, one of the leading causes of inherited mental retardation. Delayed dendritic spine maturation was found in fragile X mental retardation patients as well as in Fmr1 knockout (KO) mice, indicating the functional requirement of FMRP in synaptic development. However, the biochemical link between FMRP deficiency and the neuronal impairment during brain development has not been defined. How FMRP governs normal synapse development in the brain remains elusive. We report here that the developmentally programmed FMRP expression represses the translation of microtubule associated protein 1B (MAP1B) and is required for the accelerated decline of MAP1B during active synaptogenesis in neonatal brain development. The lack of FMRP results in misregulated MAP1B translation and delayed MAP1B decline in the Fmr1 KO brain. Furthermore, the aberrantly elevated MAP1B protein expression leads to abnormally increased microtubule stability in Fmr1 KO neurons. Together, these results indicate that FMRP plays critical roles in controlling cytoskeleton organization during neuronal development, and the abnormal microtubule dynamics is a conceivable underlying factor for the pathogenesis of fragile X mental retardation.T he absence of fragile X mental retardation protein (FMRP), a messenger ribonucleoprotein (mRNP) associated with a subclass of brain mRNAs, results in fragile X mental retardation, affecting 1 in 4,000 males and 1 in 8,000 females (1-3). The lack of FMRP results in delayed dendritic spine maturation in fragile X patients as well as in Fmr1 knockout (KO) mice (4-8), indicating the essential role of FMRP in synapse development. Furthermore, the association of FMRP with translating polyribosomes (9-12) and micro-RNA machinery (13) suggests that FMRP governs translation efficiency of its mRNA targets, which in turn modulates synaptic development and plasticity.FMRP has been shown to act as a translation repressor for its associated mRNAs in vitro as well as in cultured cell lines (14-17). To date, Ͼ400 mRNAs have been identified to associate with FMRP in vivo (18-21). In fragile X patient cells and synaptoneurosomes isolated from the Fmr1 KO brain, the lack of FMRP causes abnormal polyribosome-association of several mRNAs that normally bind to FMRP (18,21). Consistent with the proposed function of FMRP in regulating translation in synaptic plasticity, activity-dependent production of the synaptic protein PSD95 is abrogated in the Fmr1 KO primary neuronal cultures (22). In addition, the mRNA of the microtubuleassociated protein 1B (MAP1B), a neuronal MAP playing principle roles in neurite and synapse development (23), is a predicted target of FMRP (18,19,21). Interestingly, deficiency of Drosophila Fmr1 (dFmr1) results in abnormally elevated expression of the microtubule associated protein Futsch and synaptic over growth at the neuromuscular...

SUMMARYThe WRKY transcription factors have been demonstrated to play crucial roles in regulating stress responses; however, the exact mechanisms underlying their involvement in stress responses are not fully understood. Arabidopsis WRKY8 was predominantly expressed in roots and was highly upregulated by salt treatment. Disruption of WRKY8 rendered plants hypersensitive to salt, showing delayed germination, inhibited postgermination development and accelerated chlorosis. Further investigation revealed that WRKY8 interacted with VQ9, and their interaction decreased the DNA-binding activity of WRKY8. The VQ9 protein was exclusively localized in the nucleus, and VQ9 expression was strongly responsive to NaCl treatment. Mutation of VQ9 enhanced tolerance to salt stress, indicating that VQ9 acts antagonistically with WRKY8 to mediate responses to salt stress. The antagonist functions of WRKY8 and VQ9 were consistent with an increased or reduced Na + /K + concentration ratio, as well as contrasting expression patterns of downstream stressresponsive genes in salt-stressed wrky8 and vq9 mutants. Moreover, chromatin immunoprecipitation (ChIP) assays showed that WRKY8 directly bound the promoter of RD29A under salt conditions. These results provided strong evidence that the VQ9 protein acts as a repressor of the WRKY8 factor to maintain an appropriate balance of WRKY8-mediated signaling pathways to establish salinity stress tolerance.

Plants are challenged with numerous abiotic stresses, such as drought, cold, heat, and salt stress. These environmental stresses are major causes of crop failure and reduced yields worldwide. Phytohormones play essential roles in regulating various plant physiological processes and alleviating stressful perturbations. Jasmonate (JA), a group of oxylipin compounds ubiquitous in the plant kingdom, acts as a crucial signal to modulate multiple plant processes. Recent studies have shown evidence supporting the involvement of JA in leaf senescence and tolerance to cold stress. Concentrations of JA are much higher in senescent leaves compared with those in non-senescent ones. Treatment with exogenous JA induces leaf senescence and expression of senescence-associated genes. In response to cold stress, exogenous application of JA enhances Arabidopsis freezing tolerance with or without cold acclimation. Consistently, biosynthesis of endogenous JA is activated in response to cold exposure. JA positively regulates the CBF (C-REPEAT BINDING FACTOR) transcriptional pathway to up-regulate downstream cold-responsive genes and ultimately improve cold tolerance. JA interacts with other hormone signaling pathways (such as auxin, ethylene, and gibberellin) to regulate leaf senescence and tolerance to cold stress. In this review, we summarize recent studies that have provided insights into JA-mediated leaf senescence and cold-stress tolerance.

Rapid antigen tests, such as the Abbott BinaxNOW COVID-19 Ag Card (BinaxNOW), offer results more rapidly (approximately 15-30 minutes) and at a lower cost than do highly sensitive nucleic acid amplification tests (NAATs) (1). Rapid antigen tests have received Food and Drug Administration (FDA) Emergency Use Authorization (EUA) for use in symptomatic persons (2), but data are lacking on test performance in asymptomatic persons to inform expanded screening testing to rapidly identify and isolate infected persons (3). To evaluate the performance of the BinaxNOW rapid antigen test, it was used along with real-time reverse transcription-polymerase chain reaction (RT-PCR) testing to analyze 3,419 paired specimens collected from persons aged ≥10 years at two community testing sites in Pima County, Arizona, during November 3-17, 2020. Viral culture was performed on 274 of 303 residual real-time RT-PCR specimens with positive results by either test (29 were not available for culture). Compared with real-time RT-PCR testing, the BinaxNOW antigen test had a sensitivity of 64.2% for specimens from symptomatic persons and 35.8% for specimens from asymptomatic persons, with near 100% specificity in specimens from both groups. Virus was cultured from 96 of 274 (35.0%) specimens, including 85 (57.8%) of 147 with concordant antigen and real-time RT-PCR positive results, 11 (8.9%) of 124 with false-negative antigen test results, and none of three with false-positive antigen test results. Among specimens positive for viral culture, sensitivity was 92.6% for symptomatic and 78.6% for asymptomatic individuals. When the pretest probability for receiving positive test results for SARS-CoV-2 is elevated (e.g., in symptomatic persons or in persons with a known COVID-19 exposure), a negative antigen test result should be confirmed by NAAT (1). Despite a lower sensitivity to detect infection, rapid antigen tests can be an important tool for screening because of their quick turnaround time, lower costs and resource needs, high specificity, and high positive predictive value (PPV) in settings * Specimens were used to perform a limiting-dilution inoculation of Vero CCL-81 cells, and cultures showing evidence of cytopathic effect were tested by real-time RT-PCR for the presence of SARS-CoV-2 RNA. Viral recovery was defined as any culture in which the first passage had an N1 Ct value at least two Ct values lower than the corresponding clinical specimen. † https://www.biorxiv

In plants, photoperiod is an important cue for determining flowering. The floral transition in Arabidopsis thaliana is earlier under long-day (LD) than under short-day (SD) conditions. Flowering of Arabidopsis plants under SD conditions is mainly regulated by the plant hormone gibberellin (GA). Here, we report two WRKY transcription factors function oppositely in controlling flowering time under SD conditions. Phenotypic analysis showed that disruption of WRKY12 caused a delay in flowering, while loss of WRKY13 function promoted flowering. WRKY12 and WRKY13 displayed negatively correlated expression profiles and function successively to regulate flowering. Molecular and genetic analyses demonstrated that FRUITFULL (FUL) is a direct downstream target gene of WRKY12 and WRKY13. Interestingly, we found that DELLA proteins GIBBERELLIN INSENSITIVE (GAI) and RGA-LIKE1 (RGL1) interacted with WRKY12 and WRKY13, and their interactions interfered with the transcriptional activity of the WRKY12 and WRKY13. Further studies suggested thatWRKY12 and WRKY13 partly mediated the effect of GA on controlling flowering time. Taken together, our results indicate that WRKY12 and WRKY13 oppositely modulate flowering time under SD conditions, which at least partially involves the action of GA.