Microspore and pollen development in six male-sterile mutants of Arabidopsis thaliana

1993 ◽  
Vol 71 (4) ◽  
pp. 629-638 ◽  
Author(s):  
J. Dawson ◽  
Z. A. Wilson ◽  
M. G. M. Aarts ◽  
A. F. Braithwaite ◽  
L. G. Briarty ◽  
...  

Five new recessive male-sterile mutants of Arabidopsis thaliana were isolated following seed mutagenesis by X-rays and ethyl methanesulfonate. The cytology of plants homozygous for the msY and msW mutations suggested that pollen development in these lines became abnormal at or before meiosis. The msK mutation caused faulty timing of synthesis or turnover and distribution of callose. In plants homozygous for the msZ mutation, pollen development failed at a late stage. In wild-type plants, the stamen filament elongated just prior to anther dehiscence. In contrast, in the msZ mutant stamen elongation did not occur. Pollen in msH homozygotes was fertile, but anthers failed to dehisce. The msI mutant of J.H. Van der Ween and P. Wirtz (1968. Euphytica 17: 371 – 377) was included in the present study. Pollen development in this mutant failed shortly after microspore release from tetrads. Complementation tests confirmed that the ms mutations were at different loci. Reduced transmission of certain ms genes was observed. Key words: Arabidopsis thaliana, male sterile mutants, anther dehiscence, callose, inheritance.

1994 ◽  
Vol 72 (3) ◽  
pp. 384-401 ◽  
Author(s):  
Wilson Crone ◽  
Elizabeth M. Lord

The flowers of Arabidopsis thaliana (Brassicaceae) were examined for histological events during organ initiation and later development. An inflorescence floral plastochron of the main stem raceme was used as a basis for the timing and staging of developmental events. Sepals, petals, stamens, and carpels in wild-type Landsberg erecta Arabidopsis are distinguishable as primordia in terms of cell division events associated with initiation, size, and component cell numbers. Flower organogenesis in the organ identity (homeotic) mutants apetala2-1 and agamous-1 was compared with that of the wild type. In both mutants, each whorl of floral organs initiates much like the wild type and only subsequently produces visibly altered organs with mosaic features. The flower organ identity mutants achieve their mature phenotypes by alterations in tissue differentiation that occur after initiation and early primordial development. Key words: Arabidopsis, apetala2-1, agamous-1, plastochron, homeosis, flower.


2016 ◽  
Author(s):  
Gonul Dundar ◽  
Zhenhua Shao ◽  
Nahoko Higashitani ◽  
Mami Kikuta ◽  
Masanori Izumi ◽  
...  

AbstractAutophagy is one of the cellular processes that break down cellular components during senescence, starvation, and stress. The susceptibility of plant pollen development to high-temperature (HT) stress is well known, but the involvement of autophagy in HT injury is yet to be clarified. Here, we found that following transfer to 30 °C, all autophagy-deficient (atg) mutants (atg2-1, 5-1, 7-2, and 10-1) of Arabidopsis thaliana tested displayed visibly impaired pollen development and anther dehiscence. HT-induced male sterility significantly increased in the atg mutants, but the degree of HT-induced obstacles did not change between the wild type (WT) and mutants from the seedling stage to the bolting stage. Cytological analyses showed that 30 °C promoted autophagy and autolysosome formation in both anther wall cells and microspores in developing anthers of WT, but the atg5-1 mutant did not show completion of tapetum degeneration and microspore maturation. HT upregulated hydrogen peroxide and dehydroascorbate reductase 1 production in both WT and atg5-1 anthers, but the basal levels were already higher in the mutant. HT repressed expression of UNDEAD and its regulator MYB80, which are required for tapetal programmed cell death (PCD) for proper pollen development. Taken together, our results suggest that autophagy functions in tapetum degeneration and pollen development during HT-caused tapetal PCD abortion.HighlightsIn Arabidopsis, autophagy is not essential for completion of the life cycle under normal temperatures.High temperature (HT) stress induces autophagy in developing anther wall cells and microspores.Autophagy deficient atg mutants become almost completely male-sterile at moderate HT.Autophagy plays a role in tapetum degeneration and pollen development during HT-caused abortion of tapetal program cell death.


1989 ◽  
Vol 67 (10) ◽  
pp. 2922-2936 ◽  
Author(s):  
Jeffrey P. Hill ◽  
Elizabeth M. Lord

Homeosis is sometimes defined as the replacement of one member of a meristic series by another member normally formed in a different position. The pistillata floral mutant of Arabidopsis thaliana (Brassicaceae) has petals replaced by sepal-like organs ("petals"), is male sterile, and has abnormal gynoecial development. We compared the ontogeny of wild type and pistillata flowers to determine the developmental basis for their divergent final forms. Normal sepal development in wild type pistillata flowers is indistinguishable in terms of initiation events, anatomical and morphological development, and allometric growth. Wild type petals and pistillata "petals" are initially ontogenetically similar in these same respects. The first observable difference between the two floral forms is abnormal patterns of cell division in pistillata at stamen inception. Tissues in the normal position of the androecium appear congenitally fused to the gynoecium to various extents and differentiate gynoecial cell fates. Form divergence between wild type petals and pistillata "petals" becomes evident when these organs reach 90 μm in length, after androecial developmental divergence has occurred. Pistillata does not have petals replaced by sepals; pistillata "petals" are intermediate in form between wild type sepals and petals because of the developmental switching of petal primordia into the ontogenetic pattern characteristic of wild type sepals after petal primordia are initiated.


PROTOPLASMA ◽  
2002 ◽  
Vol 219 (1-2) ◽  
pp. 59-71 ◽  
Author(s):  
Chenhong Zhang ◽  
Frédérique C. Guinel ◽  
Barbara A. Moffatt

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.


1988 ◽  
Vol 8 (10) ◽  
pp. 4185-4189 ◽  
Author(s):  
J A Greenspan ◽  
F M Xu ◽  
R L Davidson

The molecular mechanisms of ethyl methanesulfonate-induced reversion in mammalian cells were studied by using as a target a gpt gene that was integrated chromosomally as part of a shuttle vector. Murine cells containing mutant gpt genes with single base changes were mutagenized with ethyl methanesulfonate, and revertant colonies were isolated. Ethyl methanesulfonate failed to increase the frequency of revertants for cell lines with mutant gpt genes carrying GC----AT transitions or AT----TA transversions, whereas it increased the frequency 50-fold to greater than 800-fold for cell lines with mutant gpt genes carrying AT----GC transitions and for one cell line with a GC----CG transversion. The gpt genes of 15 independent revertants derived from the ethyl methanesulfonate-revertible cell lines were recovered and sequenced. All revertants derived from cell lines with AT----GC transitions had mutated back to the wild-type gpt sequence via GC----AT transitions at their original sites of mutation. Five of six revertants derived from the cell line carrying a gpt gene with a GC----CG transversion had mutated via GC----AT transition at the site of the original mutation or at the adjacent base in the same triplet; these changes generated non-wild-type DNA sequences that code for non-wild-type amino acids that are apparently compatible with xanthine-guanine phosphoribosyltransferase activity. The sixth revertant had mutated via CG----GC transversion back to the wild-type sequence. The results of this study define certain amino acid substitutions in the xanthine-guanine phosphoribosyltransferase polypeptide that are compatible with enzyme activity. These results also establish mutagen-induced reversion analysis as a sensitive and specific assay for mutagenesis in mammalian cells.


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