Background Cerebrospinal fluid (CSF) is an ultra-filtrated colorless brain fluid that circulates within brain spaces like the ventricular cavities, subarachnoid space, and the spine. Its continuous flow serves many primary functions, including nourishment, brain protection, and waste removal. Main body The abnormal accumulation of CSF in brain cavities triggers severe hydrocephalus. Accumulating evidence had indicated that synchronized beats of motile cilia (cilia from multiciliated cells or the ependymal lining in brain ventricles) provide forceful pressure to generate and restrain CSF flow and maintain overall CSF circulation within brain spaces. In humans, the disorders caused by defective primary and/or motile cilia are generally referred to as ciliopathies. The key role of CSF circulation in brain development and its functioning has not been fully elucidated. Conclusions In this review, we briefly discuss the underlying role of motile cilia in CSF circulation and hydrocephalus. We have reviewed cilia and ciliated cells in the brain and the existing evidence for the regulatory role of functional cilia in CSF circulation in the brain. We further discuss the findings obtained for defective cilia and their potential involvement in hydrocephalus. Furthermore, this review will reinforce the idea of motile cilia as master regulators of CSF movements, brain development, and neuronal diseases.

Trichoderma is an important biocontrol agent for managing plant diseases. Trichoderma species are members of the fungal genus hyphomycetes, which is widely distributed in soil. It can function as a biocontrol agent as well as a growth promoter. Trichoderma species are now frequently used as biological control agents (BCAs) to combat a wide range of plant diseases. Major plant diseases have been successfully managed due to their application. Trichoderma spp. is being extensively researched in order to enhance its effectiveness as a top biocontrol agent. The activation of numerous regulatory mechanisms is the major factor in Trichoderma ability to manage plant diseases. Trichoderma-based biocontrol methods include nutrient competition, mycoparasitism, the synthesis of antibiotic and hydrolytic enzymes, and induced plant resistance. Trichoderma species may synthesize a variety of secondary metabolites that can successfully inhibit the activity of numerous plant diseases. GPCRs (G protein-coupled receptors) are membrane-bound receptors that sense and transmit environmental inputs that affect fungal secondary metabolism. Related intracellular signalling pathways also play a role in this process. Secondary metabolites produced by Trichoderma can activate disease-fighting mechanisms within plants and protect against pathogens. β- Glucuronidase (GUS), green fluorescent protein (gfp), hygromycin B phosphotransferase (hygB), and producing genes are examples of exogenous markers that could be used to identify and track specific Trichoderma isolates in agro-ecosystems. More than sixty percent of the biofungicides now on the market are derived from Trichoderma species. These fungi protect plants from harmful plant diseases by developing resistance. Additionally, they can solubilize plant nutrients to boost plant growth and bioremediate environmental contaminants through mechanisms, including mycoparasitism and antibiosis. Enzymes produced by the genus Trichoderma are frequently used in industry. This review article intends to provide an overview update (from 1975 to 2022) of the Trichoderma biocontrol fungi, as well as information on key secondary metabolites, genes, and interactions with plant diseases.

Fibroblast growth factors (FGFs) comprise a large family of growth factors, regulating diverse biological processes including cell proliferation, migration, and differentiation. Each FGF binds to a set of FGF receptors to initiate certain intracellular signaling molecules. Accumulated evidence suggests that in early development and adult state of vertebrates, FGFs also play exclusive and context dependent roles. Although FGFs have been the focus of research for therapeutic approaches in cancer, cardiovascular disease, and metabolic syndrome, in this review, we mainly focused on their role in germ layer specification and axis patterning during early vertebrate embryogenesis. We discussed the functional roles of FGFs and their interacting partners as part of the gene regulatory network for germ layer specification, dorsal–ventral (DV), and anterior-posterior (AP) patterning. Finally, we briefly reviewed the regulatory molecules and pharmacological agents discovered that may allow modulation of FGF signaling in research.

Inhibition of the bone morphogenetic proteins (BMPs) is the primary step toward neuroectoderm formation in vertebrates. In this process, the Spemann organizer of the dorsal mesoderm plays a decisive role by secreting several extracellular BMP inhibitors such as Chordin (Chrd). Chrd physically interacts with BMP proteins and inhibits BMP signaling, which triggers the expression of neural-specific transcription factors (TFs), including Foxd4l1.1. Thus, Chrd induces in a BMP-inhibited manner and promotes neuroectoderm formation. However, the regulatory feedback mechanism of Foxd4l1.1 on mesodermal genes expression during germ-layer specification has not been fully elucidated. In this study, we investigated the regulatory mechanism of Foxd4l1.1 on chrd (a mesodermal gene). We demonstrate that Foxd4l1.1 inhibits chrd expression during neuroectoderm formation in two ways: First, Foxd4l1.1 directly binds to FRE (Foxd4l1.1 response elements) within the chrd promoter region to inhibit transcription. Second, Foxd4l1.1 physically interacts with Smad2 and Smad3, and this interaction blocks Smad2 and Smad3 binding to activin response elements (AREs) within the chrd promoter. Site-directed mutagenesis of FRE within the chrd(-2250) promoter completely abolished repressor activity of the Foxd4l1.1. RT-PCR and reporter gene assay results indicate that Foxd4l1.1 strongly inhibits mesoderm- and ectoderm-specific marker genes to maintain neural fate. Altogether, these results suggest that Foxd4l1.1 negatively regulates chrd transcription by dual mechanism. Thus, our study demonstrates the existence of precise reciprocal regulation of chrd transcription during neuroectoderm and mesoderm germ-layer specification in Xenopus embryos.