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Phosphate (Pi) deficiency in soil is one of the limiting factors to a growing plant due to its slow diffusion and high fixation in the rhizosphere. Brassica rapa plants were grown hydroponically under replete (P+) and deplete (P-) conditions to examine the variations in the expression of Pi responsive genes using real-time quantitative PCR (qPCR). Nine candidate reference genes were selected from the NCBI database. TATA box and SAND were selected as the most suitable reference genes under Pi-replete and Pi-deplete conditions due to their high efficiency and quality. The selected reference genes were validated by analyzing the expression of 14 target Pi responsive genes. The expression analysis of B. rapa root samples under Pi deficiency revealed the variable expression of genes; Bro18-014187 (ALMT1), a gene that is involved in organic acid exudation (OA) in the root system to promote phosphorus use efficiency (PUE) in plants, showed the highest increased (7.6-fold) under Pi-stress. Meanwhile, the expression of genes Bro18-047862 (PAP12), Bro18-038689 (MATE), Bro18-038513 (MMDH1), Bro18-004703 (SUC2), and Bro18-025411 (SUC2) increased with 3.69-fold, 1.9-fold, 1.4-fold, 3.03-fold, and 1.8-fold, respectively. Decreased gene responses were seen in Bro18-009479 (CS4), Bro18-042204 (ALMT1), and Bro18-035630 (MATE), while five other genes Bro18-039999 (PAP12), Bro18-049018 (CS4), Bro18-006954 (ALMT1), Bro18-035465 (MMDH1) and Bro18-013770 (MMDH1) remain unchanged. The whole-genome triplication (WGT) event in B. rapa led to three copies of paralog genes and transcription analysis showed the robust variation in the expression patterns of these paralog genes. Genes involved in signaling, transport, extracellular Pi scavenging, physiological function, and metabolic pathways are among the most highly expressed genes. This research provides a general overview of Pi’s influence on plant growth processes as well as presents particular experimental data on B. rapa responses to Pi deficiency.

Autism spectrum disorder (ASD) is a neurodevelopmental condition of the central nervous system (CNS) that presents with severe communication problems, impairment of social interactions, and stereotypic behaviours. Emerging studies indicate possible associations between viral infections and neurodegenerative and neurobehavioural conditions including autism. Viral infection during critical periods of early in utero neurodevelopment may lead to increased risk of autism in the offspring. This review is aimed at highlighting the association between viral infections, including viruses similar to COVID-19, and the aetiology of autism. A literature search was conducted using Pubmed, Ovid/Medline, and Google Scholar database. Relevant search terms included “rubella and autism”, “cytomegalovirus and autism”, “influenza virus and autism”, “Zika virus and autism”, “COVID-19 and autism”. Based on the search terms, a total of 141 articles were obtained and studies on infants or children with congenital or perinatal viral infection and autistic behaviour were evaluated. The possible mechanisms by which viral infections could lead to autism include direct teratogenic effects and indirect effects of inflammation or maternal immune activation on the developing brain. Brain imaging studies have shown that the ensuing immune response from these viral infections could lead to disruption of the development of brain regions and structures. Hence, long-term follow up is necessary for infants whose mothers report an inflammatory event due to viral infection at any time during pregnancy to monitor for signs of autism. Research into the role of viral infection in the development of ASD may be one avenue of improving ASD outcomes in the future. Early screening and diagnosis to detect, and maybe even prevent ASD are essential to reduce the burden of this condition.

Autism spectrum disorder (ASD) is a heterogeneous, behaviorally defined, neurodevelopmental disorder that has been modeled as a brain-based disease. The behavioral and cognitive features of ASD are associated with pervasive atypicalities in the central nervous system (CNS). To date, the exact mechanisms underlying the pathophysiology of ASD still remain unknown and there is currently no cure or effective treatment for this disorder. Many publications implicated the association of ASD with inflammation, immune dysregulation, neurotransmission dysfunction, mitochondrial impairment and cell signaling dysregulation. This review attempts to highlight evidence of the major pathophysiology of ASD including abnormalities in the brain structure and function, neuroglial activation and neuroinflammation, glutamatergic neurotransmission, mitochondrial dysfunction and mechanistic target of rapamycin (mTOR) signaling pathway dysregulation. Molecular and cellular factors that contributed to the pathogenesis of ASD and how they may affect the development and function of CNS are compiled in this review. However, findings of published studies have been complicated by the fact that autism is a very heterogeneous disorder; hence, we addressed the limitations that led to discrepancies in the reported findings. This review emphasizes the need for future studies to control study variables such as sample size, gender, age range and intelligence quotient (IQ), all of which that could affect the study measurements. Neuroinflammation or immune dysregulation, microglial activation, genetically linked neurotransmission, mitochondrial dysfunctions and mTOR signaling pathway could be the primary targets for treating and preventing ASD. Further research is required to better understand the molecular causes and how they may contribute to the pathophysiology of ASD.