Cereal crops, including triticeae species (barley, wheat, rye), as well as edible cereals (wheat, corn, rice, oat, rye, sorghum), are significant suppliers for human consumption, livestock feed, and breweries. Over the past half-century, modern varieties of cereal crops with increased yields have contributed to global food security. However, presently cultivated elite crop varieties were developed mainly for optimal environmental conditions. Thus, it has become evident that taking into account the ongoing climate changes, currently a priority should be given to developing new stress-tolerant cereal cultivars. It is necessary to enhance the accuracy of methods and time required to generate new cereal cultivars with the desired features to adapt to climate change and keep up with the world population expansion. The CRISPR/Cas9 system has been developed as a powerful and versatile genome editing tool to achieve desirable traits, such as developing high-yielding, stress-tolerant, and disease-resistant transgene-free lines in major cereals. Despite recent advances, the CRISPR/Cas9 application in cereals faces several challenges, including a significant amount of time required to develop transgene-free lines, laboriousness, and a limited number of genotypes that may be used for the transformation and in vitro regeneration. Additionally, developing elite lines through genome editing has been restricted in many countries, especially Europe and New Zealand, due to a lack of flexibility in GMO regulations. This review provides a comprehensive update to researchers interested in improving cereals using gene-editing technologies, such as CRISPR/Cas9. We will review some critical and recent studies on crop improvements and their contributing factors to superior cereals through gene-editing technologies.

• Klíčová slova
• CRISPR/Cas, Cereals, Genome editing, Morphogenic genes, Speed breeding,
• MeSH
• CRISPR-Cas systémy genetika   MeSH
• editace genu * metody   MeSH
• geneticky modifikované rostliny genetika   MeSH
• genom rostlinný genetika   MeSH
• jedlá semena * genetika   MeSH
• lidé MeSH
• šlechtění rostlin metody   MeSH
• zemědělské plodiny genetika   MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• přehledy MeSH

Bud outgrowth is controlled by environmental and endogenous factors. Through the use of the photosynthesis inhibitor norflurazon and of masking experiments, evidence is given here that light acts mainly as a morphogenic signal in the triggering of bud outgrowth and that initial steps in the light signaling pathway involve cytokinins (CKs). Indeed, in rose (Rosa hybrida), inhibition of bud outgrowth by darkness is suppressed solely by the application of CKs. In contrast, application of sugars has a limited effect. Exposure of plants to white light (WL) induces a rapid (after 3-6 h of WL exposure) up-regulation of CK synthesis (RhIPT3 and RhIPT5), of CK activation (RhLOG8), and of CK putative transporter RhPUP5 genes and to the repression of the CK degradation RhCKX1 gene in the node. This leads to the accumulation of CKs in the node within 6 h and in the bud at 24 h and to the triggering of bud outgrowth. Molecular analysis of genes involved in major mechanisms of bud outgrowth (strigolactone signaling [RwMAX2], metabolism and transport of auxin [RhPIN1, RhYUC1, and RhTAR1], regulation of sugar sink strength [RhVI, RhSUSY, RhSUC2, and RhSWEET10], and cell division and expansion [RhEXP and RhPCNA]) reveal that, when supplied in darkness, CKs up-regulate their expression as rapidly and as intensely as WL Additionally, up-regulation of CKs by WL promotes xylem flux toward the bud, as evidenced by Methylene Blue accumulation in the bud after CK treatment in the dark. Altogether, these results suggest that CKs are initial components of the light signaling pathway that controls the initiation of bud outgrowth.

• MeSH
• biologické modely MeSH
• časové faktory MeSH
• cytokininy metabolismus   farmakologie   MeSH
• meristém genetika   růst a vývoj   metabolismus   MeSH
• polymerázová řetězová reakce s reverzní transkripcí MeSH
• regulace genové exprese u rostlin účinky léků   účinky záření   MeSH
• regulátory růstu rostlin metabolismus   farmakologie   MeSH
• Rosa genetika   růst a vývoj   metabolismus   MeSH
• rostlinné proteiny genetika   metabolismus   MeSH
• signální transdukce účinky léků   genetika   účinky záření   MeSH
• světlo * MeSH
• tma MeSH
• výhonky rostlin genetika   růst a vývoj   metabolismus   MeSH
• vývojová regulace genové exprese účinky léků   účinky záření   MeSH
• xylém genetika   růst a vývoj   metabolismus   MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• cytokininy MeSH
• regulátory růstu rostlin MeSH
• rostlinné proteiny MeSH

BACKGROUND: The mechanism of IgA nephropathy (IgAN) progression remains ill-defined. In this prospective study, the prognostic role of clinical, histological and molecular markers over a 2-year follow-up was evaluated. METHODS: Fifty-one patients with biopsy-proven IgAN were followed for 24 months. Besides routine histology, the intrarenal gene expressions of cytokines and chemokines were quantified by reverse transcription quantitative real-time polymerase chain reaction, and the presence of lymphocytes and macrophages were immunohistochemically examined. RESULTS: Higher transforming growth factor-β1 and severe chronic vasculopathy (but not glomerulosclerosis, interstitial fibrosis or lymphocyte infiltrate) were associated with the IgAN progression 24 months after biopsy. The gene expression of chemokine (C-C motif) ligands 2 and 5, hepatocyte growth factor, bone morphogenic protein-7 and transforming growth factor-β1 and the interstitial infiltrate of T and B lymphocytes and macrophages were significantly associated with serum creatinine and glomerular filtration rate at the time of biopsy. The intrarenal chemokine (C-C motif) ligand 2 and hepatocyte growth factor gene expression were associated with the proteinuria. CONCLUSIONS: Besides the known risk factors for chronic kidney disease, advanced vasculopathy and molecular signatures of fibrogenesis were associated with the IgAN progression.

• MeSH
• biopsie MeSH
• dospělí MeSH
• exprese genu MeSH
• IgA nefropatie genetika   patologie   MeSH
• ledviny patologie   MeSH
• lidé středního věku MeSH
• lidé MeSH
• následné studie MeSH
• nemoci cév genetika   patologie   MeSH
• prognóza MeSH
• progrese nemoci MeSH
• prospektivní studie MeSH
• průřezové studie MeSH
• transformující růstový faktor beta1 genetika   MeSH
• Check Tag
• dospělí MeSH
• lidé středního věku MeSH
• lidé MeSH
• mužské pohlaví MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• klinické zkoušky MeSH
• multicentrická studie MeSH
• práce podpořená grantem MeSH
• Názvy látek
• transformující růstový faktor beta1 MeSH

Sonic hedgehog (Shh) is a morphogen involved in many developmental processes. Injection of cells (5E1) that produce a Shh-blocking antibody causes an attenuation of the Shh response, and this causes vascular malformations and impaired remodeling characterized by hemorrhages and protrusions of the anterior cardinal vein and outflow tract, delayed fusion of the dorsal aortae, impaired branching of the internal carotid artery, and delayed remodeling of the aortic arches. Distribution of smooth muscle cells in the vessel wall is unchanged. In 5E1-injected embryos, we also observed impaired assembly of endothelial cells into vascular tubes, particularly in the sixth branchial arch, around the anterior cardinal vein and around the dorsal aorta. In 5E1-treated embryos, increased numbers of macrophage-like cells, apoptotic cells, and a decreased level of proliferation were observed in head mesenchyme. Together, these observations show that Shh signaling is required at multiple stages for proper vessel formation and remodeling.

• MeSH
• branchiální krajina embryologie   metabolismus   MeSH
• cévy embryologie   metabolismus   MeSH
• hybridizace in situ MeSH
• hybridomy MeSH
• imunohistochemie MeSH
• křepelky a křepelovití MeSH
• kultivované buňky MeSH
• myši MeSH
• proteiny hedgehog genetika   imunologie   metabolismus   MeSH
• protilátky imunologie   metabolismus   MeSH
• ptačí proteiny genetika   metabolismus   MeSH
• transplantace buněk MeSH
• vývojová regulace genové exprese MeSH
• zvířata MeSH
• Check Tag
• myši MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Research Support, N.I.H., Extramural MeSH
• Názvy látek
• proteiny hedgehog MeSH
• protilátky MeSH
• ptačí proteiny MeSH

Kidney vetch seedlings were induced to form hairy roots by inoculating their mesocotyls with the wild-type strain 15834 of Agrobacterium rhizogenes or with the A. tumefaciens strain C58C1 containing a binary vector system (the pRiA4b as a helper and the vector pCB1346 bearing a pTiC58-derived isopentenyl transferase gene (ipt, cytokinin biosynthetic gene) under control of its native regulatory sequences). Transgenic lines of three distinct phenotypes were selected: (i) Typically, the pRi15834-transformed tissues were stabilized in vitro and maintained for long periods as aseptic, fast-growing, hormone-independent, plagiotropic hairy root cultures which never regenerated shoots and lost the ability to synthesize opines. Their genomic DNA contained both the TL- and the TR-DNA. (ii) One of the HR-lines transgenic for the T-DNA of pRi15834 (named 52AV34) started to regenerate spontaneously into teratomous shoots. The shoots were found to produce opines and both the TL and TR parts of T-DNA were found to be partly deleted and/or rearranged. They contained phytohormones in similar levels as those found in seed-born shoots. (iii) A practically identical morphogenic response as in the line 52AV34 was observed in the clone 27AV46. However, its shooty, dark-green, slow-growing teratomas were proven to be kanamycin-resistant, opine-producing, and double-transformed by the pRiA4b sequences and the ipt gene. They over-produced auxins as well as cytokinins (mainly indoleacetylaspartic acid and ribosides of zeatin and isopentenyladenine).

• Publikační typ
• časopisecké články MeSH

The patterning of repeated structures is a major theme in developmental biology, and the inter-relationship between spacing and size of such structures is an unresolved issue. Fungiform papillae are repeated epithelial structures that house taste buds on the anterior tongue. Here, we report that FGF signaling is a crucial regulator of fungiform papillae development. We found that mesenchymal FGF10 controls the size of the papillary area, while overall patterning remains unchanged. Our results show that FGF signaling negatively affects the extent of canonical Wnt signaling, which is the main activation pathway during fungiform papillae development; however, this effect does not occur at the level of gene transcription. Rather, our experimental data, together with computational modeling, indicate that FGF10 modulates the range of Wnt effects, likely via induction of Sostdc1 expression. We suggest that modification of the reach of Wnt signaling could be due to local changes in morphogen diffusion, representing a novel mechanism in this tissue context, and we propose that this phenomenon might be involved in a broader array of mammalian developmental processes.

• Klíčová slova
• FGF, Taste papilla, Tongue, Wnt,
• MeSH
• adaptorové proteiny signální transdukční MeSH
• biologické modely MeSH
• chuťové pohárky embryologie   metabolismus   MeSH
• fibroblastový růstový faktor 10 nedostatek   genetika   metabolismus   MeSH
• intracelulární signální peptidy a proteiny nedostatek   genetika   metabolismus   MeSH
• kostní morfogenetické proteiny genetika   metabolismus   MeSH
• membránové proteiny nedostatek   genetika   metabolismus   MeSH
• myši knockoutované MeSH
• myši transgenní MeSH
• myši MeSH
• počítačová simulace MeSH
• protein-serin-threoninkinasy MeSH
• proteiny hedgehog genetika   metabolismus   MeSH
• rozvržení tělního plánu genetika   fyziologie   MeSH
• signální dráha Wnt * MeSH
• těhotenství MeSH
• zvířata MeSH
• Check Tag
• mužské pohlaví MeSH
• myši MeSH
• těhotenství MeSH
• ženské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• adaptorové proteiny signální transdukční MeSH
• Fgf10 protein, mouse MeSH Prohlížeč
• fibroblastový růstový faktor 10 MeSH
• intracelulární signální peptidy a proteiny MeSH
• kostní morfogenetické proteiny MeSH
• membránové proteiny MeSH
• protein-serin-threoninkinasy MeSH
• proteiny hedgehog MeSH
• Shh protein, mouse MeSH Prohlížeč
• Sostdc1 protein, mouse MeSH Prohlížeč
• Spry2 protein, mouse MeSH Prohlížeč

The p53 family member p63 exists as two major protein variants (TAp63 and ΔNp63) with distinct expression patterns and functional properties. Whilst downstream target genes of p63 have been studied intensively, how p63 variants are themselves controlled has been relatively neglected. Here, we review advances in understanding ΔNp63 and TAp63 regulation, highlighting their distinct pathways. TAp63 has roles in senescence and metabolism, and in germ cell genome maintenance, where it is activated post-transcriptionally by phosphorylation cascades after DNA damage. The function and regulation of TAp63 in mesenchymal and haematopoietic cells is less clear but may involve epigenetic control through DNA methylation. ΔNp63 functions to maintain stem/progenitor cells in various epithelia and is overexpressed in squamous and certain other cancers. ΔNp63 is transcriptionally regulated through multiple enhancers in concert with chromatin modifying proteins. Many signalling pathways including growth factors, morphogens, inflammation, and the extracellular matrix influence ΔNp63 levels, with inconsistent results reported. There is also evidence for reciprocal regulation, including ΔNp63 activating its own transcription. ΔNp63 is downregulated during cell differentiation through transcriptional regulation, while post-transcriptional events cause proteasomal degradation. Throughout the review, we identify knowledge gaps and highlight discordances, providing potential explanations including cell-context and cell-matrix interactions. Identifying individual p63 variants has roles in differential diagnosis and prognosis, and understanding their regulation suggests clinically approved agents for targeting p63 that may be useful combination therapies for selected cancer patients. © 2021 The Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.

• Klíčová slova
• HDAC inhibitors, chromatin modification, gene enhancers, p63, squamous cell cancer, stem cells,
• MeSH
• lidé MeSH
• nádorové supresorové proteiny * MeSH
• nádory * MeSH
• protein - isoformy MeSH
• transkripční faktory * MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• přehledy MeSH
• Názvy látek
• nádorové supresorové proteiny * MeSH
• protein - isoformy MeSH
• TP63 protein, human MeSH Prohlížeč
• transkripční faktory * MeSH