scholarly journals Endosperm development is an autonomously programmed process independent of embryogenesis

2020 ◽  
Author(s):  
Hanxian Xiong ◽  
Wei Wang ◽  
Meng-Xiang Sun

AbstractThe seeds of land plants contain three genetically distinct structures: the embryo, endosperm, and seed coat. The embryo and endosperm need to interact and exchange signals to ensure coordinated growth. Accumulating evidence has confirmed that embryo growth is supported by the nourishing endosperm and regulated by signals originating from the endosperm. Available data also support that endosperm development requires communication with the embryo. Here, using single-fertilization mutants, Arabidopsis dmp8/9 and gex2, we demonstrate that in the absence of a zygote and embryo, endosperm initiation, syncytium formation, free nuclear cellularization, and endosperm degeneration are as normal as in the wild type in terms of the cytological process and time course. Although rapid embryo expansion accelerates endosperm breakdown, our findings strongly suggest that endosperm development is an autonomously organized process, independent of egg cell fertilization and embryo–endosperm communication. This work confirms both the altruistic and self-directed nature of the endosperm during coordinated embryo-endosperm development. The findings provide novel insights into the intricate interaction between the two fertilization products and will help to distinguish the real roles of the signaling between endosperm and embryo. These finding also shed new light on agro-biotechnology for crop improvement.

Microbiology ◽  
2010 ◽  
Vol 156 (8) ◽  
pp. 2336-2342 ◽  
Author(s):  
M. Marchal ◽  
R. Briandet ◽  
S. Koechler ◽  
B. Kammerer ◽  
P. N. Bertin

Herminiimonas arsenicoxydans is a Gram-negative bacterium able to detoxify arsenic-contaminated environments by oxidizing arsenite [As(III)] to arsenate [As(V)] and by scavenging arsenic ions in an extracellular matrix. Its motility and colonization behaviour have been previously suggested to be influenced by arsenite. Using time-course confocal laser scanning microscopy, we investigated its biofilm development in the absence and presence of arsenite. Arsenite was shown to delay biofilm initiation in the wild-type strain; this was partly explained by its toxicity, which caused an increased growth lag time. However, this delayed adhesion step in the presence of arsenite was not observed in either a swimming motility defective fliL mutant or an arsenite oxidase defective aoxB mutant; both strains displayed the wild-type surface properties and growth capacities. We propose that during the biofilm formation process arsenite acts on swimming motility as a result of the arsenite oxidase activity, preventing the switch between planktonic and sessile lifestyles. Our study therefore highlights the existence, under arsenite exposure, of a competition between swimming motility, resulting from arsenite oxidation, and biofilm initiation.


2021 ◽  
Vol 2 (3) ◽  
pp. 502-516
Author(s):  
Archa Vijay ◽  
Ashifa Nizam ◽  
Arun Madasseril Radhakrishnan ◽  
Thattantavide Anju ◽  
Arun Kumar Kashyap ◽  
...  

The ovules inside the ovary of a plant are the precursors of seeds and they are important for the perpetuation of the plants. The genus Passiflora L., produce fruits with numerous seeds and they have economic and medicinal value. The edible portion of the Passiflora are the seeds surrounded by pulp. Being the edible parts of a fruit, it is important to investigate the early development of ovules in Passiflora that lead to the formation of seeds after pollination. Wild relatives of the domesticated crops are increasingly being investigated for possible genetic resources that can be used for crop improvement programs. The present study was designed to investigate the comparative ovule development between a wild (Passiflora foetida L.) and a cultivated (Passiflora edulis Sims) species of Passiflora with an aim that it may provide important information about the common and diverging regulatory mechanisms during ovule development between the wild and the cultivated species. We also investigated the pollen morphology between the wild and cultivated species using light and scanning electron microscopy. Our results show that wild type P. foetida ovule growth is faster when compared with that of cultivated P. edulis. Furthermore, wild species harbour ovules of large size (0.14 mm2) but less in number (6) as compared to cultivated ones which show smaller size (0.05 mm2) of ovules but relatively more in number (21). The differences in ovary wall thickness were also stark between the two species. The ovary wall thickness was 0.10 mm in the wild type whereas it was 0.74 mm in cultivated species. Notable differences were also observed in diameter where the wild type (2.45 mm) reported smaller diameter than cultivated species (3.25 mm). We observed little difference in the pollen morphology between the two species.


2019 ◽  
Vol 16 (1) ◽  
Author(s):  
Erica M. Weekman ◽  
Tiffany L. Sudduth ◽  
Brittani R. Price ◽  
Abigail E. Woolums ◽  
Danielle Hawthorne ◽  
...  

Abstract Background Vascular contributions to cognitive impairment and dementia (VCID) are the second leading cause of dementia behind only Alzheimer’s disease (AD); however, VCID is commonly found as a co-morbidity with sporadic AD. We have previously established a mouse model of VCID by inducing hyperhomocysteinemia in both wild-type and amyloid depositing mice. While we have shown the time course of neuropathological events in the wild-type mice with hyperhomocysteinemia, the effect of amyloid deposition on this time course remains unknown; therefore, in this study, we determined the time course of neuropathological changes in our mouse model of hyperhomocysteinemia-induced VCID in amyloid depositing mice. Methods APP/PS1 mice were placed on either a diet deficient in folate and vitamins B6 and B12 and enriched in methionine to induce hyperhomocysteinemia or a control diet for 2, 6, 10, 14, or 18 weeks. Immunohistochemistry and gene expression analysis were used to determine neuroinflammatory changes. Microhemorrhages and amyloid deposition were analyzed using histology and, finally, behavior was assessed using the 2-day radial arm water maze. Results Neuroinflammation, specifically a pro-inflammatory phenotype, was the first pathological change to occur. Specifically, we see a significant increase in gene expression of tumor necrosis factor alpha, interleukin 1 beta, interleukin 6, and interleukin 12a by 6 weeks. This was followed by cognitive deficits starting at 10 weeks. Finally, there is a significant increase in the number of microhemorrhages at 14 weeks on diet as well as redistribution of amyloid from the parenchyma to the vasculature. Conclusions The time course of these pathologies points to neuroinflammation as the initial, key player in homocysteine-induced VCID co-morbid with amyloid deposition and provides a possible therapeutic target and time points.


2001 ◽  
Vol 28 (4) ◽  
pp. 307 ◽  
Author(s):  
Adriana Chiappetta ◽  
Walter de Witte ◽  
Milvia L. Racchi ◽  
Maria B. Bitonti ◽  
Henri van Onckelen ◽  
...  

The distribution of cytokinins is strongly altered in seedlings of the shootless ed*41 mutant of maize (Zea mays L.), compared with wild-type. Immunolocalisation of zeatin and analysis of cytokinin levels clearly indicate that these hormones are not present in the shoot apex zone of the mutant. Since an anomalous differentiation of vascular tissues has also been observed in the mutant, a major role of vascular connection in hormone translocation affecting development of the shoot apical meristem is proposed. Immunolocalisation of zeatin was confined to the root cap, cortex and vascular tissues of both mutant and wild-type seedlings suggesting a tissue-specific synthesis of this hormone in the root. A time-course of cytokinin distribution in the wild-type developing shoot provided evidence that the tunica and corpus zones become competent to respond to cytokinins in subsequent periods, very probably in conjunction with photomorphogenesis. On the contrary, this pathway is totally disrupted in the mutant. Taken together, the data point to a relationship between the ed*41 mutation, inadequate vascular connection and disrupted hormone translocation.


2005 ◽  
Vol 187 (1) ◽  
pp. 286-295 ◽  
Author(s):  
Jun-ya Kato ◽  
Won-Jae Chi ◽  
Yasuo Ohnishi ◽  
Soon-Kwang Hong ◽  
Sueharu Horinouchi

ABSTRACT AdpA is the key transcriptional activator for a number of genes of various functions in the A-factor regulatory cascade in Streptomyces griseus, forming an AdpA regulon. Trypsin-like activity was detected at a late stage of growth in the wild-type strain but not in an A-factor-deficient mutant. Consistent with these observations, two trypsin genes, sprT and sprU, in S. griseus were found to be members of the AdpA regulon; AdpA activated the transcription of both genes by binding to the operators located at about −50 nucleotide positions with respect to the transcriptional start point. The transcription of sprT and sprU, induced by AdpA, was most active at the onset of sporulation. Most trypsin activity exerted by S. griseus was attributed to SprT, because trypsin activity in an sprT-disrupted mutant was greatly reduced but that in an sprU-disrupted mutant was only slightly reduced. This was consistent with the observation that the amount of the sprT mRNA was much greater than that of the sprU transcript. Disruption of both sprT and sprU (mutant ΔsprTU) reduced trypsin activity to almost zero, indicating that no trypsin genes other than these two were present in S. griseus. Even the double mutant ΔsprTU grew normally and developed aerial hyphae and spores over the same time course as the wild-type strain.


1999 ◽  
Vol 90 (2) ◽  
pp. 470-476 ◽  
Author(s):  
Tian-Zhi Guo ◽  
Frances M. Davies ◽  
Wade S. Kingery ◽  
Andrew J. Patterson ◽  
Lee E. Limbird ◽  
...  

Background Opiate receptors in the periaqueductal gray region and alpha2 adrenoceptors in the spinal cord of the rat mediate the antinociceptive properties of nitrous oxide (N2O). The availability of genetically altered mice facilitates the detection of the precise protein species involved in the transduction pathway. In this study, the authors establish the similarity between rats and mice in the antinociceptive action of N2O and investigate which alpha2 adrenoceptor subtypes mediate this response. Methods After obtaining institutional approval, antinociceptive dose-response and time-course to N2O was measured in wild-type and transgenic mice (D79N), with a nonfunctional alpha2A adrenoceptor using tail-flick latency. The antinociceptive effect of N2O was tested after pretreatment systemically with yohimbine (nonselective alpha2 antagonist), naloxone (opiate antagonist), L659,066 (peripheral alpha2-antagonist) and prazosin (alpha2B- and alpha2C-selective antagonist). The tail-flick latency to dexmedetomidine (D-med), a nonselective alpha2 agonist, was tested in wild-type and transgenic mice. Results N2O produced antinociception in both D79N transgenic and wild-type litter mates, although the response was less pronounced in the transgenic mice. Antinociception from N2O decreased over time with continuing exposure, and the decrement was more pronounced in the transgenic mice. The antinociceptive response could be dose dependently antagonized by opiate receptor and selective alpha2B-/alpha2C-receptor antagonists but not by a central nervous system-impermeant alpha2 antagonist (L659,066). Whereas dexmedetomidine exhibited no antinociceptive response in the D79N mice, the robust antinociceptive response in the wild-type litter mates could not be blocked by a selective alpha2B-/alpha2C-receptor antagonist. Conclusion These data confirm that the antinociceptive response to an exogenous alpha2-agonist is mediated by an alpha2A adrenoceptor and that there appears to be a role for the alpha2B- or alpha2C-adrenoceptor subtypes, or both, in the analgesic response to N2O.


2006 ◽  
Vol 5 (10) ◽  
pp. 1688-1704 ◽  
Author(s):  
Iran Malavazi ◽  
Marcela Savoldi ◽  
Sônia Marli Zingaretti Di Mauro ◽  
Carlos Frederico Martins Menck ◽  
Steven D. Harris ◽  
...  

ABSTRACT We have used an Aspergillus nidulans macroarray carrying sequences of 2,787 genes from this fungus to monitor gene expression of both wild-type and uvsB ATR (the homologue of the ATR gene) deletion mutant strains in a time course exposure to camptothecin (CPT). The results revealed a total of 1,512 and 1,700 genes in the wild-type and uvsB ATR deletion mutant strains that displayed a statistically significant difference at at least one experimental time point. We characterized six genes that have increased mRNA expression in the presence of CPT in the wild-type strain relative to the uvsB ATR mutant strain: fhdA (encoding a forkhead-associated domain protein), tprA (encoding a hypothetical protein that contains a tetratrico peptide repeat), mshA (encoding a MutS homologue involved in mismatch repair), phbA (encoding a prohibitin homologue), uvsC RAD51 (the homologue of the RAD51 gene), and cshA (encoding a homologue of the excision repair protein ERCC-6 [Cockayne's syndrome protein]). The induced transcript levels of these genes in the presence of CPT require uvsB ATR. These genes were deleted, and surprisingly, only the ΔuvsC mutant strain was sensitive to CPT; however, the others displayed sensitivity to a range of DNA-damaging and oxidative stress agents. These results indicate that the selected genes when inactivated display very complex and heterogeneous sensitivity behavior during growth in the presence of agents that directly or indirectly cause DNA damage. Moreover, with the exception of UvsC, deletion of each of these genes partially suppressed the sensitivity of the ΔuvsB strain to menadione and paraquat. Our results provide the first insight into the overall complexity of the response to DNA damage in filamentous fungi and suggest that multiple pathways may act in parallel to mediate DNA repair.


2000 ◽  
Vol 182 (9) ◽  
pp. 2438-2444 ◽  
Author(s):  
Lisa Gorski ◽  
Thomas Gronewold ◽  
Dale Kaiser

ABSTRACT Insertion of an internal DNA fragment into the act1gene, which encodes one of several ς54-activator proteins in Myxococcus xanthus, produced a mutant defective in fruiting body development. While fruiting-body aggregation appears normal in the mutant, it fails to sporulate (<10−6 the wild-type number of viable spores). The A and C intercellular signals, which are required for sporulation, are produced by the mutant. But, while it produces A-factor at levels as high as that of the wild type, the mutant produces much less C-signal than normal, as measured either by C-factor bioassay or by the total amount of C-factor protein detected with specific antibody. Expression of three C-factor-dependent reporters is altered in the mutant: the level of expression of Ω4414 is about 15% of normal, and Ω4459 and Ω4403 have alterations in their time course. Finally, the methylation of FrzCD protein is below normal in the mutant. It is proposed that Act1 protein responds to C-signal reception by increasing the expression of the csgAgene. This C-signal-dependent increase constitutes a positive feedback in the wild type. The act1 mutant, unable to raise the level of csgA expression, carries out only those developmental steps for which a low level of C-signaling is adequate.


1980 ◽  
Vol 84 (1) ◽  
pp. 57-71 ◽  
Author(s):  
Y. Satow ◽  
C. Kung

Membrane currents were recorded from the wild type and two pawn mutants of the pwA complementation group in Paramecium tetraurelia under a voltage clamp. Most currents are not changed by the mutations. Transient inward currents of a leaky mutant, pwA132, upon step depolarizations are less than those in the wild type. The inward transient is completely lacking in a non-leaky mutant, pwA500. The time course of the residual inward currents in the leaky mutant is not significantly different from that of wild type. The voltage sensitivity of the Ca channels in the leaky mutant is also similar to that of wild type. The inward currents upon membrane hyperpolarizations in the mutants show normal characteristics in the presence or absence of external K+. With sufficiently large, prolonged depolarization, outward currents progressively develop in the wild type but decay in the mutants. The simplest conclusion we can draw is that the pwA mutations reduce the number of functional Ca channels but do not change the channel characteristics. From the conductance measurements, 45% of the Ca channels remain in the leaky mutant pwA132, and none remain in the non-leaky mutant pwA500. By subtracting the outward currents of pwA500 from the slow and prolonged outward currents of the wild type, we have tentatively separated a Ca-induced K+ current from the voltage-dependent K+ current. The time courses of these two currents differ by two orders of magnitude.


1990 ◽  
Vol 68 (7) ◽  
pp. 1382-1389 ◽  
Author(s):  
Thomas J. Diefenbach ◽  
Jeffrey I. Goldberg

In a laboratory-reared albino strain of the snail Helisoma trivolvis, the number of neurons expressing the serotonin phenotype increases markedly during postembryonic life. To address whether these latent changes occur selectively in the laboratory-reared strain, postembryonic expression of serotonin immunoreactivity was directly compared in laboratory-reared and wild-type specimens. The spatial pattern of serotonin-immunoreactive neurons was generally the same in the two strains. In contrast, the time course over which this pattern was generated was more prolonged in the wild types than in the laboratory-reared strain. The cerebral, left parietal, and visceral ganglia of laboratory-reared animals completed their postembryonic acquisition of serotonin-immunoreactive neurons by stage P10. Acquisition of serotonin-immunoreactive neurons after stage P10 occurred only in the pedal ganglia. In the wild types, addition of serotonin-immunoreactive neurons continued at least until stage P20 in all of the ganglia examined. Analysis of serotonergic clusters within the cerebral and pedal ganglia revealed distinct developmental patterns for individual clusters. Therefore, the acquisition of the serotonin phenotype during postembryonic life is a normal component of nervous system development in wild-type H. trivolvis.


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