In multicellular organisms, controlling the timing and extent of asymmetric cell divisions (ACDs) is crucial for correct patterning. During post-embryonic root development in Arabidopsis thaliana, ground tissue (GT) maturation involves an additional ACD of the endodermis, which generates two different tissues: the endodermis (inner) and the middle cortex (outer). It has been reported that the abscisic acid (ABA) and gibberellin (GA) pathways are involved in middle cortex (MC) formation. However, the molecular mechanisms underlying the interaction between ABA and GA during GT maturation remain largely unknown. Through transcriptome analyses, we identified a previously uncharacterized C2H2-type zinc finger gene, whose expression is regulated by GA and ABA, thus named GAZ (GA- AND ABA-RESPONSIVE ZINC FINGER). Seedlings ectopically overexpressing GAZ (GAZ-OX) were sensitive to ABA and GA during MC formation, whereas GAZ-SRDX and RNAi seedlings displayed opposite phenotypes. In addition, our results indicated that GAZ was involved in the transcriptional regulation of ABA and GA homeostasis. In agreement with previous studies that ABA and GA coordinate to control the timing of MC formation, we also confirmed the unique interplay between ABA and GA and identified factors and regulatory networks bridging the two hormone pathways during GT maturation of the Arabidopsis root.
Development of the functional endodermis of Arabidopsis thaliana roots is controlled, in part, by GRAS transcription factors, namely SHORT-ROOT (SHR), SCARECROW (SCR), and SCARECROW-LIKE 23 (SCL23). Recently, it has been shown that the SHR-SCR-SCL23 regulatory module is also essential for specification of the endodermis (known as the bundle sheath) in leaves. Nevertheless, compared with what is known about the role of the SHR-SCR-SCL23 regulatory network in roots, the molecular interactions of SHR, SCR, and SCL23 are much less understood in shoots. Here, we show that SHR forms protein complexes with SCL23 to regulate transcription of SCL23 in shoots, similar to the regulation mode of SCR expression. Our results indicate that SHR acts as master regulator to directly activate the expression of SCR and SCL23. In the SHR-SCR-SCL23 network, we found a previously uncharacterized negative feedback loop whereby SCL23 modulates SHR levels. Through molecular, genetic, physiological, and morphological analyses, we also reveal that the SHR-SCR-SCL23 module plays a key role in the formation of the endodermis (known as the starch sheath) in hypocotyls. Taken together, our results provide new insights into the regulatory role of the SHR-SCR-SCL23 network in the endodermis development in both roots and shoots.
When perceiving microbe-associated molecular patterns (MAMPs) or plant-derived damage-associated molecular patterns (DAMPs), plants alter their root growth and development by displaying a reduction in the root length and the formation of root hairs and lateral roots. The exogenous application of a MAMP peptide, flg22, was shown to affect root growth by suppressing meristem activity. In addition to MAMPs, the DAMP peptide PEP1 suppresses root growth while also promoting root hair formation. However, the question of whether and how these elicitor peptides affect the development of the vascular system in the root has not been explored. The cellular receptors of PEP1, PEPR1 and PEPR2 are highly expressed in the root vascular system, while the receptors of flg22 ( FLS2 ) and elf18 ( EFR ) are not. Consistent with the expression patterns of PEP1 receptors, we found that exogenously applied PEP1 has a strong impact on the division of stele cells, leading to a reduction of these cells. We also observed the alteration in the number and organization of cells that differentiate into xylem vessels. These PEP1-mediated developmental changes appear to be linked to the blockage of symplastic connections triggered by PEP1. PEP1 dramatically disrupts the symplastic movement of free green fluorescence protein (GFP) from phloem sieve elements to neighboring cells in the root meristem, leading to the deposition of a high level of callose between cells. Taken together, our first survey of PEP1-mediated vascular tissue development provides new insights into the PEP1 function as a regulator of cellular reprogramming in the Arabidopsis root vascular system.
Transcriptional regulation, a core component of gene regulatory networks, plays a key role in controlling individual organism's growth and development. To understand how plants modulate cellular processes for growth and development, the identification and characterization of gene regulatory networks are of importance. The SHORT-ROOT (SHR) transcription factor is known for its role in cell divisions in Arabidopsis (Arabidopsis thaliana). However, whether SHR is involved in hypocotyl cell elongation remains unknown. Here, we reveal that SHR controls hypocotyl cell elongation via the transcriptional regulation of XTH18, XTH22, and XTH24, which encode cell wall remodeling enzymes called xyloglucan endotransglucosylase/hydrolases (XTHs). Interestingly, SHR activates transcription of the XTH genes, independently of its partner SCARECROW (SCR), which is different from the known mode of action. In addition, overexpression of the XTH genes can promote cell elongation in the etiolated hypocotyl. Moreover, confinement of SHR protein in the stele still induces cell elongation, despite the aberrant organization in the hypocotyl ground tissue. Therefore, it is likely that SHR-mediated growth is uncoupled from SHR-mediated radial patterning in the etiolated hypocotyl. Our findings also suggest that intertissue communication between stele and endodermis plays a role in coordinating hypocotyl cell elongation of the Arabidopsis seedling. Taken together, our study identifies SHR as a new crucial regulator that is necessary for cell elongation in the etiolated hypocotyl.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.