A rice heterochronic mutant, mori1, is defective in the juvenile-adult phase change

Development ◽  
2002 ◽  
Vol 129 (1) ◽  
pp. 265-273 ◽  
Author(s):  
Kazumi Asai ◽  
Namiko Satoh ◽  
Haruto Sasaki ◽  
Hikaru Satoh ◽  
Yasuo Nagato

We have identified five recessive allelic mutations, mori1-1 to mori1-5, which drastically modify the shoot architecture of rice. The most remarkable feature of mori1 plants is a rapid production of small leaves and short branches. The mori1 plants are about 5 cm in height even 7 months after sowing. No reproductive growth was attained in mori1 plants even if inductive short-day treatment was applied. Leaves of mori1 at any position were very small and the size and shape were comparable to those of the wild-type 2nd leaf. The stem of mori1 7 months after sowing did not differentiate node and internode and had randomly oriented vascular bundles, which were characteristic of the basal part of the wild-type stem where 2nd and 3rd leaves were inserted. These structural characteristics indicate that mori1 maintains the 2nd-leaf stage (juvenile phase) of the wild type. The short plastochron and high cell division activity in the shoot apical meristem further confirmed the juvenility of mori1, corresponding to the 2nd-leaf-differentiation stage in the wild-type embryo. Furthermore, the apparent photosynthetic rate in mori1 leaves was low as in the wild-type 2nd leaf. Thus, mori1 is a heterochronic mutation that suppresses the induction of adult phase and the termination of the juvenile phase. Therefore, MORI1 plays an important role in the juvenile-adult phase change. The importance of heterochronic mutations in modifying shoot architecture is discussed.

Development ◽  
1994 ◽  
Vol 120 (7) ◽  
pp. 1971-1981 ◽  
Author(s):  
M.M. Evans ◽  
H.J. Passas ◽  
R.S. Poethig

Vegetative development in maize is divided into a juvenile phase and an adult phase that differ in the expression of a large number of morphological, anatomical, and biochemical traits. Recessive mutations of Glossy15 cause a premature switch in the expression of some of these phase-specific traits. Mutant plants cease producing juvenile traits (e.g. epicuticular wax) and begin to produce adult traits (e.g. epidermal hairs) significantly earlier than their wild-type siblings. In glossy15-1 plants this switch generally occurs at leaf 2 or 3 rather than at the normal position of leaf 6 or 7. An analysis of the effect of glossy15 mutations on a variety of vegetative and reproductive traits revealed that these mutations only affect the character of the epidermis. They have no effect on the overall vegetative morphology of the plant, or on its reproductive development. This phenotype is the opposite of that of the gain-of-function mutations Teopod1, Teopod2 and Teopod3, all of which prolong the expression of a large number of juvenile traits. Double mutants between glossy15 and Teopod1 or Teopod2 indicate that Glossy15 is required for the effect of Teopod1 and Teopod2 on epidermal traits but not for other aspects of the Teopod phenotype. We conclude that Glossy15 initiates or maintains the expression of juvenile epidermal traits and suppresses the expression of adult epidermal traits, and that it acts downstream of the Teopod genes.


2006 ◽  
Vol 52 (4) ◽  
pp. 328-335 ◽  
Author(s):  
Puji Lestari ◽  
Kyujung Van ◽  
Moon Young Kim ◽  
Byun-Woo Lee ◽  
Suk-Ha Lee

Supernodulating soybean (Glycine max L. Merr.) mutant SS2-2 and its wild-type counterpart, Sinpaldalkong 2, were examined for the microstructural events associated with nodule formation and development. SS2-2 produced a substantially higher percentage of curled root hairs than the wild type, especially at 14 days after inoculation with Bradyrhizobium japonicum. In addition, there was new evidence that in SS2-2, B. japonicum also entered through fissures created by the emerging adventitious root primordia. Early steps of nodule ontogeny were faster in SS2-2, and continued development of initiated nodules was more frequent and occurred at a higher frequency than in the wild type. These data suggest that the early expression of autoregulation is facilitated by decreasing the speed of cortical cell development, leading to the subsequent termination of less-developed nodules. The nodules of SS2-2 developed into spherical nodules like those formed on the wild type. In both the wild type and supernodulating mutant, vascular bundles bifurcate from root stele and branch off in the nodule cortex to surround the central infected zone. These findings indicate that SS2-2 has complete endosymbiosis and forms completely developed nodule vascular bundles like the wild type, but that the speed of nodule ontogeny differs between the wild type and SS2-2. Thus, SS2-2 has a novel symbiotic phenotype with regard to nodule organogenesis.Key words: Bradyrhizobium japonicum, early nodule development, Glycine max, root hair curling, supernodulation.


2021 ◽  
Vol 118 (12) ◽  
pp. e2019631118
Author(s):  
Máximo Sanz-Hernández ◽  
Joseph D. Barritt ◽  
Jens Sobek ◽  
Simone Hornemann ◽  
Adriano Aguzzi ◽  
...  

The misfolding and aggregation of the human prion protein (PrP) is associated with transmissible spongiform encephalopathies (TSEs). Intermediate conformations forming during the conversion of the cellular form of PrP into its pathological scrapie conformation are key drivers of the misfolding process. Here, we analyzed the properties of the C-terminal domain of the human PrP (huPrP) and its T183A variant, which is associated with familial forms of TSEs. We show that the mutation significantly enhances the aggregation propensity of huPrP, such as to uniquely induce amyloid formation under physiological conditions by the sole C-terminal domain of the protein. Using NMR spectroscopy, biophysics, and metadynamics simulations, we identified the structural characteristics of the misfolded intermediate promoting the aggregation of T183A huPrP and the nature of the interactions that prevent this species to be populated in the wild-type protein. In support of these conclusions, POM antibodies targeting the regions that promote PrP misfolding were shown to potently suppress the aggregation of this amyloidogenic mutant.


Development ◽  
1986 ◽  
Vol 92 (1) ◽  
pp. 255-268
Author(s):  
S. K. Frost ◽  
L. G. Epp ◽  
S. J. Robinson

The albino mutant in the Mexican axolotl (Ambystoma mexicanum) is analysed with respect to the differentiation of pigment cells. Pigment cells were observed with the transmission electron microscope in order to determine any unusual structural characteristics and to determine what happens to each of the cell types as development proceeds. Chemical analyses of pteridine pigments were also carried out, and the pattern of pteridines in albino animals was found to be more complex than, and quantitatively enhanced (at all developmental stages examined) over, the pattern observed in comparable wild-type axolotls. The golden colour of albino axolotls is due primarily to sepiapterin (a yellow pteridine) and secondarily to riboflavin (and other flavins). Coincident with enhanced levels of yellow pigments, xanthophore pigment organelles (pterinosomes) in albino skin reach a mature state earlier than they do in wild-type axolotl skin. This morphology is conserved throughout development in albino animals whereas it is gradually lost in the wild type. Unpigmented melanophores from albino axolotls are illustrated for the first time, and in larval albino axolotls the morphology of these cells is shown to be very similar to xanthophore morphology. In older albino animals xanthophores are easily distinguished from unpigmented melanophores. Iridophores seem to appear in albino skin at an earlier stage than they have been observed in wild-type skin. Morphologically, wild-type and albino iridophores are identical.


2019 ◽  
Vol 116 (28) ◽  
pp. 14319-14324 ◽  
Author(s):  
Jingbo Duan ◽  
Hong Yu ◽  
Kun Yuan ◽  
Zhigang Liao ◽  
Xiangbing Meng ◽  
...  

Strigolactones (SLs), a group of terpenoid lactones derived from carotenoids, are plant hormones that control numerous aspects of plant development. Although the framework of SL signaling that the repressor DWARF 53 (D53) could be SL-dependently degraded via the SL receptor D14 and F-box protein D3 has been established, the downstream response genes to SLs remain to be elucidated. Here we show that the cytokinin (CK) content is dramatically increased in shoot bases of the rice SL signaling mutantd53. By examining transcript levels of all the CK metabolism-related genes after treatment with SL analog GR24, we identifiedCYTOKININ OXIDASE/DEHYDROGENASE 9(OsCKX9) as a primary response gene significantly up-regulated within 1 h of treatment in the wild type but not ind53. We also found that OsCKX9 functions as a cytosolic and nuclear dual-localized CK catabolic enzyme, and that the overexpression ofOsCKX9suppresses the browning ofd53calli. Both the CRISPR/Cas9-generatedOsCKX9mutants andOsCKX9-overexpressing transgenic plants showed significant increases in tiller number and decreases in plant height and panicle size, suggesting that the homeostasis ofOsCKX9plays a critical role in regulating rice shoot architecture. Moreover, we identified the CK-inducible rice type-A response regulatorOsRR5as the secondary SL-responsive gene, whose expression is significantly repressed after 4 h of GR24 treatment in the wild type but not inosckx9. These findings reveal a comprehensive plant hormone cross-talk in which SL can induce the expression ofOsCKX9to down-regulate CK content, which in turn triggers the response of downstream genes.


Author(s):  
Thecan Caesar-Ton That ◽  
Lynn Epstein

Nectria haematococca mating population I (anamorph, Fusarium solani) macroconidia attach to its host (squash) and non-host surfaces prior to germ tube emergence. The macroconidia become adhesive after a brief period of protein synthesis. Recently, Hickman et al. (1989) isolated N. haematococca adhesion-reduced mutants. Using freeze substitution, we compared the development of the macroconidial wall in the wild type in comparison to one of the mutants, LEI.Macroconidia were harvested at 1C, washed by centrifugation, resuspended in a dilute zucchini fruit extract and incubated from 0 - 5 h. During the incubation period, wild type macroconidia attached to uncoated dialysis tubing. Mutant macroconidia did not attach and were collected on poly-L-lysine coated dialysis tubing just prior to freezing. Conidia on the tubing were frozen in liquid propane at 191 - 193C, substituted in acetone with 2% OsO4 and 0.05% uranyl acetate, washed with acetone, and flat-embedded in Epon-Araldite. Using phase contrast microscopy at 1000X, cells without freeze damage were selected, remounted, sectioned and post-stained sequentially with 1% Ba(MnO4)2 2% uranyl acetate and Reynold’s lead citrate. At least 30 cells/treatment were examined.


2007 ◽  
Vol 28 (3) ◽  
pp. 897-906 ◽  
Author(s):  
Thomas J. Pohl ◽  
Jac A. Nickoloff

ABSTRACT Homologous recombination (HR) is critical for DNA double-strand break (DSB) repair and genome stabilization. In yeast, HR is catalyzed by the Rad51 strand transferase and its “mediators,” including the Rad52 single-strand DNA-annealing protein, two Rad51 paralogs (Rad55 and Rad57), and Rad54. A Rad51 homolog, Dmc1, is important for meiotic HR. In wild-type cells, most DSB repair results in gene conversion, a conservative HR outcome. Because Rad51 plays a central role in the homology search and strand invasion steps, DSBs either are not repaired or are repaired by nonconservative single-strand annealing or break-induced replication mechanisms in rad51Δ mutants. Although DSB repair by gene conversion in the absence of Rad51 has been reported for ectopic HR events (e.g., inverted repeats or between plasmids), Rad51 has been thought to be essential for DSB repair by conservative interchromosomal (allelic) gene conversion. Here, we demonstrate that DSBs stimulate gene conversion between homologous chromosomes (allelic conversion) by >30-fold in a rad51Δ mutant. We show that Rad51-independent allelic conversion and break-induced replication occur independently of Rad55, Rad57, and Dmc1 but require Rad52. Unlike DSB-induced events, spontaneous allelic conversion was detected in both rad51Δ and rad52Δ mutants, but not in a rad51Δ rad52Δ double mutant. The frequencies of crossovers associated with DSB-induced gene conversion were similar in the wild type and the rad51Δ mutant, but discontinuous conversion tracts were fivefold more frequent and tract lengths were more widely distributed in the rad51Δ mutant, indicating that heteroduplex DNA has an altered structure, or is processed differently, in the absence of Rad51.


Genetics ◽  
1996 ◽  
Vol 142 (2) ◽  
pp. 383-391 ◽  
Author(s):  
Yasumasa Tsukamoto ◽  
Jun-ichi Kato ◽  
Hideo Ikeda

Abstract To examine the mechanism of illegitimate recombination in Saccharomyces cerevisiae, we have developed a plasmid system for quantitative analysis of deletion formation. A can1 cyh2 cell carrying two negative selection markers, the CAN1 and CYH2 genes, on a YCp plasmid is sensitive to canavanine and cycloheximide, but the cell becomes resistant to both drugs when the plasmid has a deletion over the CAN1 and CYH2 genes. Structural analysis of the recombinant plasmids obtained from the resistant cells showed that the plasmids had deletions at various sites of the CAN1-CYH2 region and there were only short regions of homology (1-5 bp) at the recombination junctions. The results indicated that the deletion detected in this system were formed by illegitimate recombination. Study on the effect of several rad mutations showed that the recombination rate was reduced by 30-, 10-, 10-, and 10-fold in the rad52, rad50, mre11, and xrs2 mutants, respectively, while in the rud51, 54, 55, and 57 mutants, the rate was comparable to that in the wild-type strain. The rad52 mutation did not affect length of homology at junction sites of illegitimate recombination.


Genes ◽  
2021 ◽  
Vol 12 (5) ◽  
pp. 618
Author(s):  
Yue Jin ◽  
Shihao Li ◽  
Yang Yu ◽  
Chengsong Zhang ◽  
Xiaojun Zhang ◽  
...  

A mutant of the ridgetail white prawn, which exhibited rare orange-red body color with a higher level of free astaxanthin (ASTX) concentration than that in the wild-type prawn, was obtained in our lab. In order to understand the underlying mechanism for the existence of a high level of free astaxanthin, transcriptome analysis was performed to identify the differentially expressed genes (DEGs) between the mutant and wild-type prawns. A total of 78,224 unigenes were obtained, and 1863 were identified as DEGs, in which 902 unigenes showed higher expression levels, while 961 unigenes presented lower expression levels in the mutant in comparison with the wild-type prawns. Based on Gene Ontology analysis and Kyoto Encyclopedia of Genes and Genomes analysis, as well as further investigation of annotated DEGs, we found that the biological processes related to astaxanthin binding, transport, and metabolism presented significant differences between the mutant and the wild-type prawns. Some genes related to these processes, including crustacyanin, apolipoprotein D (ApoD), cathepsin, and cuticle proteins, were identified as DEGs between the two types of prawns. These data may provide important information for us to understand the molecular mechanism of the existence of a high level of free astaxanthin in the prawn.


Genetics ◽  
1998 ◽  
Vol 149 (2) ◽  
pp. 565-577
Author(s):  
Daniel B Szymanski ◽  
Daniel A Klis ◽  
John C Larkin ◽  
M David Marks

Abstract In Arabidopsis, the timing and spatial arrangement of trichome initiation is tightly regulated and requires the activity of the GLABROUS1 (GL1) gene. The COTYLEDON TRICHOME 1 (COT1) gene affects trichome initiation during late stages of leaf development and is described in this article. In the wild-type background, cot1 has no observable effect on trichome initiation. GL1 overexpression in wild-type plants leads to a modest number of ectopic trichomes and to a decrease in trichome number on the adaxial leaf surface. The cot1 mutation enhances GL1-overexpression-dependent ectopic trichome formation and also induces increased leaf trichome initiation. The expressivity of the cot1 phenotype is sensitive to cot1 and 35S::GL1 gene dosage, and the most severe phenotypes are observed when cot1 and 35S::GL1 are homozygous. The COT1 locus is located on chromosome 2 15.3 cM north of er. Analysis of the interaction between cot1, try, and 35S::GL1 suggests that COT1 is part of a complex signal transduction pathway that regulates GL1-dependent adoption of the trichome cell fate.


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