SHORT-ROOT Stabilizes PHOSPHATE1 to Regulate Phosphate Allocation in Arabidopsis

Abstract Coordinated distribution of Pi between roots and shoots is an important process that plants use to maintain Pi homeostasis. SHR (SHORT-ROOT) is well-characterized for its function in root radial patterning1-3. Here, we demonstrate a new role of SHR in controlling phosphate (Pi) allocation from roots to shoots by regulating PHOSPHATE1 (PHO1) in the root differentiation zone. We recovered a weak mutant allele of SHR in Arabidopsis which accumulates much less Pi in the shoot and shows constitutive Pi starvation response (PSR) under Pi-sufficient condition. Besides, Pi starvation suppresses SHR protein accumulation and releases its inhibition on the HD-ZIP Ⅲ transcription factor PHB. PHB accumulates and directly binds the promoter of PHO2 to upregulate its transcription, resulting in PHO1 degradation in the xylem-pole pericycle cells. Our findings reveal a previously unrecognized mechanism of how plants repress Pi translocation from roots to shoots in response to Pi starvation.

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Expression Pattern Suggests a Role of MiR399 in the Regulation of the Cellular Response to Local Pi Increase During Arbuscular Mycorrhizal Symbiosis

Molecular Plant-Microbe Interactions ◽

10.1094/mpmi-23-7-0915 ◽

2010 ◽

Vol 23 (7) ◽

pp. 915-926 ◽

Cited By ~ 101

Author(s):

Anja Branscheid ◽

Daniela Sieh ◽

Bikram Datt Pant ◽

Patrick May ◽

Emanuel A. Devers ◽

...

Keyword(s):

Cellular Response ◽

Arbuscular Mycorrhizal ◽

Am Fungi ◽

Mycorrhizal Symbiosis ◽

Pi Homeostasis ◽

Pi Starvation ◽

Mycorrhizal Roots ◽

Am Symbiosis ◽

Pi Stress

Many plants improve their phosphate (Pi) availability by forming mutualistic associations with arbuscular mycorrhizal (AM) fungi. Pi-repleted plants are much less colonized by AM fungi than Pi-depleted plants. This indicates a link between plant Pi signaling and AM development. MicroRNAs (miR) of the 399 family are systemic Pi-starvation signals important for maintenance of Pi homeostasis in Arabidopsis thaliana and might also qualify as signals regulating AM development in response to Pi availability. MiR399 could either represent the systemic low-Pi signal promoting or required for AM formation or they could act as counter players of systemic Pi-availability signals that suppress AM symbiosis. To test either of these assumptions, we analyzed the miR399 family in the AM-capable plant model Medicago truncatula and could experimentally confirm 10 novel MIR399 genes in this species. Pi-depleted plants showed increased expression of mature miR399 and multiple pri-miR399, and unexpectedly, levels of five of the 15 pri-miR399 species were higher in leaves of mycorrhizal plants than in leaves of nonmycorrhizal plants. Compared with nonmycorrhizal Pi-depleted roots, mycorrhizal roots of Pi-depleted M. truncatula and tobacco plants had increased Pi contents due to symbiotic Pi uptake but displayed higher mature miR399 levels. Expression levels of MtPho2 remained low and PHO2-dependent Pi-stress marker transcript levels remained high in these mycorrhizal roots. Hence, an AM symbiosis-related signal appears to increase miR399 expression and decrease PHO2 activity. MiR399 overexpression in tobacco suggested that miR399 alone is not sufficient to improve mycorrhizal colonization supporting the assumption that, in mycorrhizal roots, increased miR399 are necessary to keep the MtPho2 expression and activity low, which would otherwise increase in response to symbiotic Pi uptake.

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MULTIPLE ALLELE APPROACH TO THE STUDY OF GENES IN DROSOPHILA MELANOGASTER THAT ARE INVOLVED IN IMAGINAL DISC DEVELOPMENT

Genetics ◽

10.1093/genetics/89.2.355 ◽

1978 ◽

Vol 89 (2) ◽

pp. 355-370 ◽

Cited By ~ 2

Author(s):

Allen Shearn ◽

Grafton Hersperger ◽

Evelyn Hersperger ◽

Ellen Steward Pentz ◽

Paul Denker

Keyword(s):

Drosophila Melanogaster ◽

Phenotypic Variation ◽

Mutant Allele ◽

Imaginal Disc ◽

Reference Allele ◽

Multiple Allele ◽

Significant Difference ◽

Chromosome Mutations ◽

Cold Sensitive

ABSTRACT The phenotypes of five different lethal mutants of Drosophila melanogaster that have small imaginal discs were analyzed in detail. From these results, we inferred whether or not the observed imaginal disc phenotype resulted exclusively from a primary imaginal disc defect in each mutant. To examine the validity of these inferences, we employed a multiple-allele method. Lethal alleles of the five third-chromosome mutations were identified by screening EMS-treated chromosomes for those which fail to complement with a chromosome containing all five reference mutations. Twenty-four mutants were isolated from 13,197 treated chromosomes. Each of the 24 was then tested for complementation with each of the five reference mutants. There was no significant difference in the mutation frequencies at these five loci. The stage of lethality and the imaginal disc morphology of each mutant allele were compared to those of its reference allele in order to examine the range of defects to be found among lethal alleles of each locus. In addition, hybrids of the alleles were examined for intracistronic complementation. For two of the five loci, we detected no significant phenotypic variation among lethal alleles. We infer that each of the mutant alleles at these two loci cause expression of the null activity phenotype. However, for the three other loci, we did detect significant phenotypic variation among lethal alleles. In fact, one of the mutant alleles at each of these three loci causes no detectable imaginal disc defect. This demonstrates that attempting to assess the developmental role of a gene by studying a single mutant allele may lead to erroneous conclusions. As a byproduct of the mutagenesis procedure, we have isolated two dominant, cold-sensitive mutants.

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The segment polarity gene armadillo interacts with the wingless signaling pathway in both embryonic and adult pattern formation

Development ◽

10.1242/dev.111.4.1029 ◽

1991 ◽

Vol 111 (4) ◽

pp. 1029-1043 ◽

Cited By ~ 42

Author(s):

M. Peifer ◽

C. Rauskolb ◽

M. Williams ◽

B. Riggleman ◽

E. Wieschaus

Keyword(s):

Pattern Formation ◽

Imaginal Discs ◽

Protein Accumulation ◽

Segment Polarity Genes ◽

Adult Pattern ◽

Segment Polarity ◽

Lethal Allele ◽

Segment Polarity Gene ◽

Polarity Gene

The segment polarity genes of Drosophila were initially defined as genes required for pattern formation within each embryonic segment. Some of these genes also function to establish the pattern of the adult cuticle. We have examined the role of the armadillo (arm) gene in this latter process. We confirmed and extended earlier findings that arm and the segment polarity gene wingless are very similar in their effects on embryonic development. We next discuss the role of arm in pattern formation in the imaginal discs, as determined by using a pupal lethal allele, by analyzing clones of arm mutant tissue in imaginal discs, and by using a transposon carrying arm to produce adults with a reduced level of arm. Together, these experiments established that arm is required for the development of all imaginal discs. The requirement for arm varies along the dorsal-ventral and proximal-distal axes. Cells that require the highest levels of arm are those that express the wingless gene. Further, animals with reduced arm levels have phenotypes that resemble those of weak alleles of wingless. We present a description of the patterns of arm protein accumulation in imaginal discs. Finally, we discuss the implications of these results for the role of arm and wingless in pattern formation.

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The role of monoamine oxidase A in HPV-16 E7-induced epithelial-mesenchymal transition and HIF-1α protein accumulation in non-small cell lung cancer cells

International Journal of Biological Sciences ◽

10.7150/ijbs.46966 ◽

2020 ◽

Vol 16 (14) ◽

pp. 2692-2703

Author(s):

Bingyu Huang ◽

Zhiyuan Zhou ◽

Jiao Liu ◽

Xin Wu ◽

Xiangyong Li ◽

...

Keyword(s):

Lung Cancer ◽

Monoamine Oxidase ◽

Cancer Cells ◽

Epithelial Mesenchymal Transition ◽

Small Cell ◽

Monoamine Oxidase A ◽

Protein Accumulation ◽

Small Cell Lung ◽

Mesenchymal Transition

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SERPINA1 Peptides in Urine as A Potential Marker of Preeclampsia Severity

International Journal of Molecular Sciences ◽

10.3390/ijms21030914 ◽

2020 ◽

Vol 21 (3) ◽

pp. 914 ◽

Cited By ~ 1

Author(s):

Natalia Starodubtseva ◽

Natalia Nizyaeva ◽

Oleg Baev ◽

Anna Bugrova ◽

Masara Gapaeva ◽

...

Keyword(s):

Trophoblast Invasion ◽

Control Group ◽

Protective Mechanism ◽

Protein Accumulation ◽

Multisystem Disorder ◽

Disease Etiology ◽

Potential Marker ◽

Diagnostic Potential ◽

Urinary Peptides

Preeclampsia (PE) is a multisystem disorder associated with pregnancy and its frequency varies from 5 to 20 percent of pregnancies. Although a number of preeclampsia studies have been carried out, there is no consensus about disease etiology and pathogenesis so far. Peptides of SERPINA1 (α1-antitrypsin) in urine remain one of the most promising peptide markers of PE. In this study the diagnostic potential of urinary α1-antitrypsin peptides in PE was evaluated. The urinary peptidome composition of 79 pregnant women with preeclampsia (PE), chronic arterial hypertension (CAH), and a control group was investigated. Mann–Whitney U-test (p < 0.05) revealed seven PE specific SERPINA1 peptides demonstrating 52% sensitivity and 100% specificity. SERPINA1 in urine has been associated with the most severe forms of preeclampsia (p = 0.014), in terms of systolic hypertension (p = 0.01) and proteinuria (p = 0.006). According to Spearman correlation analysis, the normalized intensity of SERPINA1 urinary peptides has a similar diagnostic pattern with known diagnostic PE markers, such as sFLT/PLGF. SERPINA1 peptides were not urinary excreted in superimposed PE (PE with CAH), which is a milder form of PE. An increase in expression of SERPINA1 in the structural elements of the placenta during preeclampsia reflects a protective mechanism against hypoxia. Increased synthesis of SERPINA1 in the trophoblast leads to protein accumulation in fibrinoid deposits. It may block syncytial knots and placenta villi, decreasing trophoblast invasion. Excretion of PE specific SERPINA1 peptides is associated with syncytiotrophoblast membrane destruction degradation and increased SERPINA1 staining. It confirms that the placenta could be the origin of SERPINA1 peptides in urine. Significant correlation (p < 0.05) of SERPINA1 expression in syncytiotrophoblast membrane and cytoplasm with the main clinical parameters of severe PE proves the role of SERPINA1 in PE pathogenesis. Estimation of SERPINA1 peptides in urine can be used as a diagnostic test of the severity of the condition to determine further treatment, particularly the need for urgent surgical delivery.

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Short and sweet: foreleg abnormalities in Havanese and the role of the FGF4 retrogene

Canine Medicine and Genetics ◽

10.1186/s40575-020-00097-5 ◽

2020 ◽

Vol 7 (1) ◽

Author(s):

Kim K. L. Bellamy ◽

Frode Lingaas

Keyword(s):

Mutant Allele ◽

Large Degree ◽

Population Increase ◽

Wild Type Allele ◽

Wild Type ◽

Gradual Decline ◽

Type Allele ◽

Population Frequency ◽

Welfare Implications

Abstract Background Cases of foreleg deformities, characterized by varying degrees of shortened and bowed forelegs, have been reported in the Havanese breed. Because the health and welfare implications are severe in some of the affected dogs, further efforts should be made to investigate the genetic background of the trait. A FGF4-retrogene on CFA18 is known to cause chondrodystrophy in dogs. In most breeds, either the wild type allele or the mutant allele is fixed. However, the large degree of genetic diversity reported in Havanese, could entail that both the wild type and the mutant allele segregate in this breed. We hypothesize that the shortened and bowed forelegs seen in some Havanese could be a consequence of FGF4RG-associated chondrodystrophy. Here we study the population prevalence of the wild type and mutant allele, as well as effect on phenotype. We also investigate how the prevalence of the allele associated with chondrodystrophy have changed over time. We hypothesize that recent selection, may have led to a gradual decline in the population frequency of the lower-risk, wild type allele. Results We studied the FGF4-retrogene on CFA18 in 355 Havanese and found variation in the presence/absence of the retrogene. The prevalence of the non-chondrodystrophic wild type is low, with allele frequencies of 0.025 and 0.975 for the wild type and mutant allele, respectively (linked marker). We found that carriers of the beneficial wild type allele were significantly taller at the shoulder than mutant allele homozygotes, with average heights of 31.3 cm and 26.4 cm, respectively. We further found that wild type carriers were born on average 4.7 years earlier than mutant allele homozygotes and that there has been a gradual decline in the population frequency of the wild type allele during the past two decades. Conclusions Our results indicate that FGF4RG-associated chondrodystrophy may contribute to the shortened forelegs found in some Havanese and that both the wild type and mutant allele segregate in the breed. The population frequency of the wild type allele is low and appear to be decreasing. Efforts should be made to preserve the healthier wild type in the population, increase the prevalence of a more moderate phenotype and possibly reduce the risk of foreleg pathology.

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Signaling Pathways Critical for Tooth Root Formation

Journal of Dental Research ◽

10.1177/0022034517717478 ◽

2017 ◽

Vol 96 (11) ◽

pp. 1221-1228 ◽

Cited By ~ 25

Author(s):

J. Wang ◽

J.Q. Feng

Keyword(s):

Signaling Pathways ◽

Root Formation ◽

Root Resorption ◽

Tooth Development ◽

Critical Role ◽

Future Research ◽

Tooth Root ◽

Short Root ◽

Dentin Formation

Tooth is made of an enamel-covered crown and a cementum-covered root. Studies on crown dentin formation have been a major focus in tooth development for several decades. Interestingly, the population prevalence for genetic short root anomaly (SRA) with no apparent defects in crown is close to 1.3%. Furthermore, people with SRA itself are predisposed to root resorption during orthodontic treatment. The discovery of the unique role of Nfic (nuclear factor I C; a transcriptional factor) in controlling root but not crown dentin formation points to a new concept: tooth crown and root have different control mechanisms. Further genetic mechanism studies have identified more key molecules (including Osterix, β-catenin, and sonic hedgehog) that play a critical role in root formation. Extensive studies have also revealed the critical role of Hertwig’s epithelial root sheath in tooth root formation. In addition, Wnt10a has recently been found to be linked to multirooted tooth furcation formation. These exciting findings not only fill the critical gaps in our understanding about tooth root formation but will aid future research regarding the identifying factors controlling tooth root size and the generation of a whole “bio-tooth” for therapeutic purposes. This review starts with human SRA and mainly focuses on recent progress on the roles of NFIC-dependent and NFIC-independent signaling pathways in tooth root formation. Finally, this review includes a list of the various Cre transgenic mouse lines used to achieve tooth root formation–related gene deletion or overexpression, as well as strengths and limitations of each line.

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