The HOBBIT gene is required for formation of the root meristem in the Arabidopsis embryo

Development ◽  
1998 ◽  
Vol 125 (3) ◽  
pp. 521-531 ◽  
Author(s):  
V. Willemsen ◽  
H. Wolkenfelt ◽  
G. de Vrieze ◽  
P. Weisbeek ◽  
B. Scheres

In Arabidopsis, the root meristem originates from the hypophyseal cell and from an adjoining cell tier that is distinct at the heart stage of embryogenesis. We have analysed mutations in the HOBBIT (HBT) gene that is essential for root meristem formation. hbt embryos display incorrect hypophyseal cell development from the quadrant stage onward. At the heart stage, the adjoining cell tier of hbt embryos develops abnormally, in that the activation of cell division and the formation of a lateral root cap layer are disturbed. Strong hbt mutants give rise to seedlings that lack an anatomically recognisable quiescent centre and differentiated columella root cap cells, the cell types derived from the wild-type hypophysis. Furthermore, they have no mitotically active root meristem and lack a differentiated lateral root cap. Secondary roots of hbt mutants and roots obtained from cultured cells of hbt mutants have similar defects. Therefore the HBT gene is required for root meristem formation in different developmental contexts.

Development ◽  
1994 ◽  
Vol 120 (9) ◽  
pp. 2465-2474 ◽  
Author(s):  
C. M. Duckett ◽  
C. Grierson ◽  
P. Linstead ◽  
K. Schneider ◽  
E. Lawson ◽  
...  

The development of the post-embryonic root epidermis of Arabidopsis thaliana is described. Clonal analysis has identified three sets of initials that give rise to the columella root cap cells, epidermis and lateral root-cap cells, and the cells of the cortex and endodermis respectively. The mature epidermis is composed of two cell types, root hair cells (derived from trichoblasts) and non- hair cells (derived from atrichoblasts). These cells are arranged in sixteen or more discrete files. Each hair cell file overlies the anticlinal (radial) wall of the underlying cortical cells and is separated from the next by one or two non-hair files. The root hair forms as a tip-growing projection from the basal end of the trichoblast i.e. the end nearest the root meristem. The non-hair epidermal cells are significantly longer than the hair forming cells and are located over the outer periclinal (tangential) wall of the underlying cortical cells. The size difference between the two cell types is apparent in the cell division zone before hairs form. This suggests that the signals required for the differentiation of the root epidermis function in the meristem itself. Ectopic hairs are present in the ctr1 root epidermis suggesting that a Raf protein kinase may play a role in pattern formation/differentiation in the root epidermis and that ethylene may be a diffusible signal involved in specifying pattern in the root epidermis.


Development ◽  
1995 ◽  
Vol 121 (1) ◽  
pp. 53-62 ◽  
Author(s):  
B. Scheres ◽  
L. Di Laurenzio ◽  
V. Willemsen ◽  
M. T. Hauser ◽  
K. Janmaat ◽  
...  

The primary root of Arabidopsis thaliana has a remarkably uniform cellular organisation. The fixed radial pattern of cell types in the mature root arises from proliferative divisions within the root meristem. The root meristem, in turn, is laid down during embryogenesis. We have analysed six mutations causing alterations in the radial organisation of the root. Embryonic phenotypes resulting from wooden leg, gollum, pinocchio, scarecrow, shortroot and fass mutations are described. While mutations in the fass gene affect morphogenesis of all cells, the five other mutations cause alterations in specific layers. Wooden leg and gollum mutations interfere with the proper organisation of the vascular tissue. Shortroot, scarecrow and pinocchio affect the endodermis and cortex. The layer- specific phenotypes caused by all five mutations are also apparent in the hypocotyl. All these phenotypes originate from defects in the radial organisation of the embryonic axis. Secondary roots, which are formed post-embryonically, also display layer-specific phenotypes.


2018 ◽  
Author(s):  
Mouli Ghosh Dastidar ◽  
Andrea Scarpa ◽  
Ira Mägele ◽  
Paola Ruiz-Duarte ◽  
Patrick von Born ◽  
...  

SUMMARYThe root meristem is organized around a quiescent centre surrounded by stem cells that generate all cell types of the root. In the transit amplifying compartment progeny of stem cells further divide prior to differentiation. Auxin controls the size of this transit-amplifying compartment via Auxin Response Factors (ARF) that interact with Auxin Response Elements (AuxRE) in the promoter of their targets. The microRNA miR390 regulates abundance of ARF2, ARF3 and ARF4 by triggering the production of trans-acting (ta)-siRNA from TAS3. This miR390/TAS3/ARF regulatory module confers sensitivity and robustness to auxin responses in diverse developmental contexts. Here, we show that miR390 is expressed in the transit-amplifying compartment of the root meristem where it modulates response to auxin. A single AuxRE bound by ARF5/MONOPTEROS (MP) in miR390 promoter is necessary for miR390 expression in this compartment. We show that interfering with ARF5/MP dependent auxin signaling attenuates miR390 expression in the transit-amplifying compartment. Our results show that ARF5/MP regulates directly the expression of miR390 in the basal root meristem. We propose that ARF5, miR390 and the ta-siRNAs-regulated ARFs are necessary to maintain the size of the transit-amplifying region of the meristem.One sentence summaryThe expression of miR390 in the Arabidopsis basal root meristem is controlled by ARF5/MONOPTEROS.


Genetics ◽  
2001 ◽  
Vol 158 (3) ◽  
pp. 1189-1201 ◽  
Author(s):  
William J Wolfgang ◽  
Ashwini Hoskote ◽  
Ian J H Roberts ◽  
Shannon Jackson ◽  
Michael Forte

Abstract One of the best understood signal transduction pathways activated by receptors containing seven transmembrane domains involves activation of heterotrimeric G-protein complexes containing Gsα, the subsequent stimulation of adenylyl cyclase, production of cAMP, activation of protein kinase A (PKA), and the phosphorylation of substrates that control a wide variety of cellular responses. Here, we report the identification of “loss-of-function” mutations in the Drosophila Gsα gene (dgs). Seven mutants have been identified that are either complemented by transgenes representing the wild-type dgs gene or contain nucleotide sequence changes resulting in the production of altered Gsα protein. Examination of mutant alleles representing loss-of-Gsα function indicates that the phenotypes generated do not mimic those created by mutational elimination of PKA. These results are consistent with the conclusion reached in previous studies that activation of PKA, at least in these developmental contexts, does not depend on receptor-mediated increases in intracellular cAMP, in contrast to the predictions of models developed primarily on the basis of studies in cultured cells.


Genetics ◽  
1996 ◽  
Vol 142 (3) ◽  
pp. 893-906 ◽  
Author(s):  
Elizabeth Gustavson ◽  
Andrew S Goldsborough ◽  
Zehra Ali ◽  
Thomas B Kornberg

Abstract We isolated and characterized numerous engrailed and invected alleles. Among the deficiencies we isolated, a mutant lacking invected sequences was viable and phenotypically normal, a mutant lacking engrailed was an embryo lethal and had slight segmentation defects, and a mutant lacking both engrailed and invected was most severely affected. In seven engrailed alleles, mutations caused translation to terminate prematurely in the central or C-terminal portion of the coding sequence, resulting in embryonic lethality and segmentation defects. Both engrailed and invected expression declined prematurely in these mutant embryos. In wild-type embryos, engrailed and invected are juxtaposed and are expressed in essentially identical patterns. A breakpoint mutant that separates the mgrailed and invected transcription units parceled different aspects of the expression pattern to engrailed or invected. We also found that both genes cause similar defects when expressed ectopically and that the protein products of both genes act to repress transcription in cultured cells. We propose that the varied phenotypes of the engrailed alleles can be explained by the differential effects these mutants have on the combination of engrailed and invected activities, that engrailed and invected share a regulatory region, and that they encode redundant functions.


2016 ◽  
Vol 113 (34) ◽  
pp. E4995-E5004 ◽  
Author(s):  
Wen Lu ◽  
Michael Winding ◽  
Margot Lakonishok ◽  
Jill Wildonger ◽  
Vladimir I. Gelfand

Cytoplasmic streaming in Drosophila oocytes is a microtubule-based bulk cytoplasmic movement. Streaming efficiently circulates and localizes mRNAs and proteins deposited by the nurse cells across the oocyte. This movement is driven by kinesin-1, a major microtubule motor. Recently, we have shown that kinesin-1 heavy chain (KHC) can transport one microtubule on another microtubule, thus driving microtubule–microtubule sliding in multiple cell types. To study the role of microtubule sliding in oocyte cytoplasmic streaming, we used a Khc mutant that is deficient in microtubule sliding but able to transport a majority of cargoes. We demonstrated that streaming is reduced by genomic replacement of wild-type Khc with this sliding-deficient mutant. Streaming can be fully rescued by wild-type KHC and partially rescued by a chimeric motor that cannot move organelles but is active in microtubule sliding. Consistent with these data, we identified two populations of microtubules in fast-streaming oocytes: a network of stable microtubules anchored to the actin cortex and free cytoplasmic microtubules that moved in the ooplasm. We further demonstrated that the reduced streaming in sliding-deficient oocytes resulted in posterior determination defects. Together, we propose that kinesin-1 slides free cytoplasmic microtubules against cortically immobilized microtubules, generating forces that contribute to cytoplasmic streaming and are essential for the refinement of posterior determinants.


2021 ◽  
pp. 1-10
Author(s):  
Yuki Morimoto ◽  
Takeshi Oya ◽  
Mayuko Ichimura-Shimizu ◽  
Minoru Matsumoto ◽  
Hirohisa Ogawa ◽  
...  

<b><i>Objectives:</i></b> Cytology and histology are 2 indispensable diagnostic tools for cancer diagnosis, which are rapidly increasing in importance with aging populations. We applied mass spectrometry (MS) as a rapid approach for swiftly acquiring nonmorphological information of interested cells. Conventional MS, which primarily rely on promoting ionization by pre-applying a matrix to cells, has the drawback of time-consuming both on data acquisition and analysis. As an emerging method, probe electrospray ionization-MS (PESI-MS) with a dedicated probe is capable to pierce sample and measure specimen in small amounts, either liquid or solid, without the requirement for sample pretreatment. Furthermore, PESI-MS is timesaving compared to the conventional MS. Herein, we investigated the capability of PESI-MS to characterize the cell types derived from the respiratory tract of human tissues. <b><i>Study Design:</i></b> PESI-MS analyses with DPiMS-2020 were performed on various type of cultured cells including 5 lung squamous cell carcinomas, 5 lung adenocarcinomas, 5 small-cell carcinomas, 4 malignant mesotheliomas, and 2 normal controls. <b><i>Results:</i></b> Several characteristic peaks were detected at around m/z 200 and 800 that were common in all samples. As expected, partial least squares-discriminant analysis of PESI-MS data distinguished the cancer cell types from normal control cells. Moreover, distinct clusters divided squamous cell carcinoma from adenocarcinoma. <b><i>Conclusion:</i></b> PESI-MS presented a promising potential as a novel diagnostic modality for swiftly acquiring specific cytological information.


2021 ◽  
Vol 22 (14) ◽  
pp. 7360
Author(s):  
Angie De La Cruz ◽  
Aubrey Hargrave ◽  
Sri Magadi ◽  
Justin A. Courson ◽  
Paul T. Landry ◽  
...  

Platelet extravasation during inflammation is under-appreciated. In wild-type (WT) mice, a central corneal epithelial abrasion initiates neutrophil (PMN) and platelet extravasation from peripheral limbal venules. The same injury in mice expressing low levels of the β2-integrin, CD18 (CD18hypo mice) shows reduced platelet extravasation with PMN extravasation apparently unaffected. To better define the role of CD18 on platelet extravasation, we focused on two relevant cell types expressing CD18: PMNs and mast cells. Following corneal abrasion in WT mice, we observed not only extravasated PMNs and platelets but also extravasated erythrocytes (RBCs). Ultrastructural observations of engorged limbal venules showed platelets and RBCs passing through endothelial pores. In contrast, injured CD18hypo mice showed significantly less venule engorgement and markedly reduced platelet and RBC extravasation; mast cell degranulation was also reduced compared to WT mice. Corneal abrasion in mast cell-deficient (KitW-sh/W-sh) mice showed less venule engorgement, delayed PMN extravasation, reduced platelet and RBC extravasation and delayed wound healing compared to WT mice. Finally, antibody-induced depletion of circulating PMNs prior to corneal abrasion reduced mast cell degranulation, venule engorgement, and extravasation of PMNs, platelets, and RBCs. In summary, in the injured cornea, platelet and RBC extravasation depends on CD18, PMNs, and mast cell degranulation.


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