scholarly journals Overexpression of a Novel LcKNOX Transcription Factor from Liriodendron chinense Induces Lobed Leaves in Arabidopsis thaliana

Forests ◽  
2019 ◽  
Vol 11 (1) ◽  
pp. 33
Author(s):  
Jikai Ma ◽  
Guoguo Mei ◽  
Huanhuan Liu ◽  
Huogen Li

Liriodendron chinense is a common ornamental tree that has attractive leaves, which is a valuable trait for use in landscape architecture. In this work, we aimed to identify the potential genes that control and regulate the development of L. chinense leaf lobes. Based on the transcriptome data for the leaf developmental stages we previously generated, two candidate genes were identified in this study. KNOTTED-LIKE HOMEOBOX(KNOX), encoding homeobox family proteins, play a large role in leaf lobe and leaf complexity regulation. Here, two full length KNOX genes from L. chinense were amplified and named LcKNOX1 and LcKNOX6 according to their sequence similarities with the respective Arabidopsis thaliana KNOX family genes. Overexpression vectors were constructed and subsequently transformed into wild type (WT) A. thaliana. Additionally, LcKNOX6 was expressed in tobacco leaves to examine its subcellular localization, and the 35S::LcKNOX6 transgenic A. thaliana leaf cells were imaged with the use of SEM. The expression of several genes that participate in KNOX gene regulation were validated by quantitative real-time PCR. The results show that LcKNOX1 produces almost the same phenotype as that found in WT A. thaliana. Notably, the LcKNOX6-1 lines presented deep leaf lobes that were similar to L. chinense leaf lobes. Two 35S::LcKNOX6 lines induced an abnormal growth phenotype whose seeds were abortive. In short, these results indicate that the LcKNOX6 gene might affect leaf development in A. thaliana and provide insights into the regulation of L. chinense leaf shaping.

Development ◽  
1993 ◽  
Vol 118 (3) ◽  
pp. 751-764 ◽  
Author(s):  
H. Tsukaya ◽  
S. Naito ◽  
G. P. Redei ◽  
Y. Komeda

We isolated and analyzed mutants of Arabidopsis thaliana, acaulis, with flower stalks that are almost absent or are much reduced in length. The mutations are divided between two loci, acaulis1 (acl1) and acaulis2 (acl2). The acl1-1 mutation has been assigned to linkage group 4 in the vicinity of locus ap2. The acl1-1 mutant showed premature arrest of the inflorescence meristem after the onset of reproductive development, followed by consequent reduction in the number of flower-bearing phytomers and therefore flowers. The apical meristem of the inflorescences was morphologically normal but its radius was about half that of the wild type. The acl1 mutants are also defective in the development of foliage leaves. Both defects could be rescued by growth at a specific temperature (28°C). The length of the cells in acl1-3 mutant was less than that in the wild type but the numbers of cells in leaves and internodes of acl1 mutants were calculated to be the same as those of the wild type. Thus, the defects in inflorescences and leaves were attributed to defects in the process of elongation (maturation) of these cells. Temperature-shift experiments showed that the Acl1+ product was necessary at all developmental stages. A critical stage was shown to exist for recovery from the cessation of development of inflorescence meristems that was caused by the acl1-1 mutation. Grafting experiments showed that the acl1-1 mutation does not affect diffusible substances. An analysis of double mutants carrying both acl1-1 and one of developmental mutations, ap1, clv1, lfy, or tfl1, showed that ACL1 is a new class of gene.


2002 ◽  
Vol 30 (4) ◽  
pp. 481-488 ◽  
Author(s):  
Jean-Emmanuel Faure ◽  
Nicolas Rotman ◽  
Philippe Fortune ◽  
Christian Dumas

2021 ◽  
Vol 28 (1) ◽  
Author(s):  
Veronica Giourieva ◽  
Emmanuel Panteris

Abstract Background Cortical microtubules regulate cell expansion by determining cellulose microfibril orientation in the root apex of Arabidopsis thaliana. While the regulation of cell wall properties by cortical microtubules is well studied, the data on the influence of cell wall to cortical microtubule organization and stability remain scarce. Studies on cellulose biosynthesis mutants revealed that cortical microtubules depend on Cellulose Synthase A (CESA) function and/or cell expansion. Furthermore, it has been reported that cortical microtubules in cellulose-deficient mutants are hypersensitive to oryzalin. In this work, the persistence of cortical microtubules against anti-microtubule treatment was thoroughly studied in the roots of several cesa mutants, namely thanatos, mre1, any1, prc1-1 and rsw1, and the Cellulose Synthase Interacting 1 protein (csi1) mutant pom2-4. In addition, various treatments with drugs affecting cell expansion were performed on wild-type roots. Whole mount tubulin immunolabeling was applied in the above roots and observations were performed by confocal microscopy. Results Cortical microtubules in all mutants showed statistically significant increased persistence against anti-microtubule drugs, compared to those of the wild-type. Furthermore, to examine if the enhanced stability of cortical microtubules was due to reduced cellulose biosynthesis or to suppression of cell expansion, treatments of wild-type roots with 2,6-dichlorobenzonitrile (DCB) and Congo red were performed. After these treatments, cortical microtubules appeared more resistant to oryzalin, than in the control. Conclusions According to these findings, it may be concluded that inhibition of cell expansion, irrespective of the cause, results in increased microtubule stability in A. thaliana root. In addition, cell expansion does not only rely on cortical microtubule orientation but also plays a regulatory role in microtubule dynamics, as well. Various hypotheses may explain the increased cortical microtubule stability under decreased cell expansion such as the role of cell wall sensors and the presence of less dynamic cortical microtubules.


Genetics ◽  
2000 ◽  
Vol 154 (1) ◽  
pp. 437-446 ◽  
Author(s):  
Lisa Girard ◽  
Michael Freeling

Abstract Insertions of Mutator transposons into maize genes can generate suppressible alleles. Mu suppression is when, in the absence of Mu activity, the phenotype of a mutant allele reverts to that of its progenitor. Here we present the characterization of five dominant Mu-suppressible alleles of the knox (knotted1-like homeobox) genes liguleless3 and rough sheath1, which exhibit neomorphic phenotypes in the leaves. RNA blot analysis suggests that Mu suppression affects only the neomorphic aspect of the allele, not the wild-type aspect. Additionally, Mu suppression appears to be exerting its effects at the level of transcription or transcript accumulation. We show that truncated transcripts are produced by three alleles, implying a mechanism for Mu suppression of 5′ untranslated region insertion alleles distinct from that which has been described previously. Additionally, it is found that Mu suppression can be caused by at least three different types of Mutator elements. Evidence presented here suggests that whether an allele is suppressible or not may depend upon the site of insertion. We cite previous work on the knox gene kn1, and discuss our results in the context of interactions between Mu-encoded products and the inherently negative regulation of neomorphic liguleless3 and rough sheath1 transcription.


Genetics ◽  
1996 ◽  
Vol 144 (2) ◽  
pp. 495-510 ◽  
Author(s):  
B K Haarer ◽  
A Corbett ◽  
Y Kweon ◽  
A S Petzold ◽  
P Silver ◽  
...  

Abstract Replacement of the wild-type yeast profilin gene (PFY1) with a mutated form (pfy1-111) that has codon 72 changed to encode glutamate rather than arginine results in defects similar to, but less severe than, those that result from complete deletion of the profilin gene. We have used a colony color-sectoring assay to identify mutations that cause pfy1-111, but not wild-type, cells to be inviable. These profilin synthetic lethal (psl) mutations result in various degrees of abnormal growth, morphology, and temperature sensitivity in PFY1 cells. We have examined psl1 strains in the most detail. Interestingly, these strains display a diploid-specific defect in bud-site selection; haploid strains bud normally, while homozygous diploid strains show a dramatic increase in random budding. We discovered that PSL1 is the late secretory gene, SEC3, and have found that mutations in several other late secretory genes are also synthetically lethal with pfy1-111. Our results are likely to reflect an interdependence between the actin cytoskeleton and secretory processes in directing cell polarity and growth. Moreover, they indicate that the secretory pathway is especially crucial for maintaining budding polarity in diploids.


Science ◽  
2013 ◽  
Vol 341 (6150) ◽  
pp. 1103-1106 ◽  
Author(s):  
Ruben Vanholme ◽  
Igor Cesarino ◽  
Katarzyna Rataj ◽  
Yuguo Xiao ◽  
Lisa Sundin ◽  
...  

Lignin is a major component of plant secondary cell walls. Here we describe caffeoyl shikimate esterase (CSE) as an enzyme central to the lignin biosynthetic pathway. Arabidopsis thaliana cse mutants deposit less lignin than do wild-type plants, and the remaining lignin is enriched in p-hydroxyphenyl units. Phenolic metabolite profiling identified accumulation of the lignin pathway intermediate caffeoyl shikimate in cse mutants as compared to caffeoyl shikimate levels in the wild type, suggesting caffeoyl shikimate as a substrate for CSE. Accordingly, recombinant CSE hydrolyzed caffeoyl shikimate into caffeate. Associated with the changes in lignin, the conversion of cellulose to glucose in cse mutants increased up to fourfold as compared to that in the wild type upon saccharification without pretreatment. Collectively, these data necessitate the revision of currently accepted models of the lignin biosynthetic pathway.


2010 ◽  
Vol 48 (8) ◽  
pp. 697-702 ◽  
Author(s):  
Nisreen A. AL-Quraan ◽  
Robert D. Locy ◽  
Narendra K. Singh

Botany ◽  
2010 ◽  
Vol 88 (8) ◽  
pp. 710-724 ◽  
Author(s):  
Julie Kang ◽  
Neelima R. Sinha

Formation of a compound leaf requires the involvement of multiple factors, including KNOX1 gene expression. To further characterize simple and complex tomato leaf mutants, we analyzed their morphology and development by assessing: leaf phenotypes, primary leaf morphogenesis, expression of the class I KNOX gene LeT6, and meristematic activity of the marginal blastozone. Mutants with alterations in lobing and (or) pinnation (decrease/increase) were analyzed. Primary leaflet initiation is delayed in mutants with decreased lobing. In contrast, leaflet initiation is advanced or similar to the wild type in mutants with deep lobes. Leaves with increased pinnation along the rachis require a protracted developmental program to form their final leaf morphology. Using a morphometric analysis, we show that leaf complexity can be quantified. The expression pattern of LeT6 correlates with histological analysis of meristematic activity of the marginal blastozone, suggesting that LeT6 may play a role, through some unknown mechanism, to regulate meristematic competence, not only in the marginal blastozone to regulate leaflet lobing, but along the entire length of the leaf to regulate pinnation in compound leaves.


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