Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptome analysis of male sterile maize mutants defective in somatic cell layer identities (tcl1, mtm00-06 and ms*6015) compared with fertile siblings

ABSTRACT: In order to better understand defects at the molecular level in male sterile maize mutants, we characterized 3 different mutants by microarray hybridization. Anthers were dissected and staged to be 1000 μm in length (+/- 100 μm), allowing us to analyze changes in transcriptome between siblings relatively close to the initial observation of morphological defects. All three of the mutants had morphological defects in the somatic layers of the anther, but only tcl1 and mtm00-06 male steriles show serial extra periclinal divisions compared to relatively minor defects in ms*6015 male steriles.

ORGANISM(S): Zea mays

PROVIDER: GSE78259 | GEO | 2016/07/01

SECONDARY ACCESSION(S): PRJNA313049

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Transcriptome analysis of male sterile maize mutants defective in somatic cell layer identities (tcl1, mtm00-06 and ms*6015) compared with fertile siblings

Project description:In order to better understand defects at the molecular level in male sterile maize mutants, we characterized 3 different mutants by microarray hybridization. Anthers were dissected and staged to be 1000 Î¼m in length (+/- 100 Î¼m), allowing us to analyze changes in transcriptome between siblings relatively close to the initial observation of morphological defects. All three of the mutants had morphological defects in the somatic layers of the anther, but only tcl1 and mtm00-06 male steriles show serial extra periclinal divisions compared to relatively minor defects in ms*6015 male steriles. For each mutant four biological replicates were used for both male sterile samples and fertile siblings with direct comparisons made between fertile and sterile siblings of the same mutant background.

2016-07-01 | E-GEOD-78259 | biostudies-arrayexpress

bHLH cascade regulate 24-nt phasiRNA biogenesis in maize anther

Project description:Anthers are the male reproductive floral organs, but loss of the 24-nt class of phased small-interfering RNAs (phasiRNAs) may confer temperature-sensitive male sterility in maize. 24-nt phasiRNAs from 176 loci are abundant coordinately in fertile maize anthers after the last periclinal divisions are complete, all four wall layers are formed, and meiosis has initiated in the pollen mother cells. In this study, we found male sterile maize ms23, ms32, and bhlh122 mutants with various degrees of tapetal defects lack 24-PHAS mRNA precursors and 24-nt phasiRNAs, which were not affected in another male sterile mutant, bhlh51. Transcription from most of 24-PHAS loci depends on bHLH122 while bHLH122 and Dcl5 transcription depends on both Ms23 and Ms32. Multiple lines of evidence suggest that 24-nt phasiRNAs biogenesis is primarily controlled at multiple layers by MS23 and MS32, with distinctive action on 24-PHAS transcription by bHLH122, creating a transcription factor cascade in maize tapetal cells.

2022-01-10 | GSE175915 | GEO

Microarray of zebrafish (Danio rerio) sfpq-/-;Tg(mnx1:GFP) against sfpq+/+;Tg(mnx1:GFP) and sfpq+/-;Tg(mnx1:GFP) siblings at 24 hpf

Project description:Phenotypic characterisation of our zebrafish sfpq homozygous mutants revealed a restricted set of specific defects, unexpected for a protein expressed ubiquitously and involved in such general mechanisms. The CNS was prominently affected, showing brain boundary and axonal defects associated with absence of motility. To investigate a possible specificity in SFPQ functional targets by microarray RNA profiling analysis, comparing the transcriptome of the sfpq homozygous mutants with its wild type and heterozygous siblings at the earliest stage at which the phenotype is robustly recognizable.

2017-09-01 | E-MTAB-5559 | biostudies-arrayexpress

Maize seedling mRNA-seq of splicing factor mutants and their wild-type siblings

Project description:The maize Rough endosperm3 (Rgh3) gene encodes an ortholog of the human essential splicing factor, ZRSR2. To test whether a mutation in Rgh3 affects mRNA splicing, we compared rgh3 mutants and wild-type sibling transcriptomes in an RNA-seq experiment. Twelve libraries were constructed with mRNA extracted from the roots and shoots of three seedlings of each genotype. The libraries were multiplexed and sequenced on one lane of the HiSeq 2000 platform. The run produced 149 million paired-end 100 bp reads that mapped to 35,028 genes. Two approaches were used to analyze the dataset. In the first approach, Mosaik2, FreeBayes, GSNAP, and Cufflinks were used to identify differences in transcript isoform abundance in a SNP-tolerant fashion. During reverse-transcription PCR validation, six examples of intron retention were found to occur more frequently in rgh3 seedlings, and all six introns were members of a rare class of introns called U12-type introns. The second approach utilized a t-test to determine whether more reads were mapped to U12-type introns in rgh3 libraries relative to wild-type libraries. Out of all U12-type introns within genes that are expressed at a early seedling stage, 43% exhibit splicing defects in rgh3 mutants. These U12-type intron splicing defects include intron retention and cryptic splice site activation. We report that the rgh3 mutation specifically impairs the U12-type intron splicing.

2017-02-13 | GSE57466 | GEO

Transcriptome of bhlh010, bhlh089 and bhlh091 mutant anthers

Project description:Transcriptomic analysis of single, double and triple mutant anthers of bhlh010, bhlh089 and bhlh091. We examine here three recently duplicated Arabidopsis bHLH genes, bHLH010, bHLH089 and bHLH091, using evolutionary, genetic, morphological and transcriptomic approaches, and uncover their redundant functions in anther development. These three genes are relatively highly expressed in the tapetum of the Arabidopsis anther; single mutants at each of the bHLH010, bHLH089 and bHLH091 loci are developmentally normal, but the various double and triple combinations progressively exhibit increasingly defective anther phenotypes (abnormal tapetum morphology, delayed callose degeneration, and aborted pollen development), indicating their redundant functions in male fertility. Note: Samples in SRA were assigned the same sample accession. This is incorrect as there are different samples, hence “Source Name” was replaced with new values. Comment[ENA_SAMPLE] contains the original SRA sample accessions.

2015-06-01 | E-MTAB-4277 | biostudies-arrayexpress

Functional analysis of Tcl1 using Tcl1-deficient mouse embryonic stem cells.

Project description: Not available

| S-EPMC3733782 | biostudies-literature

Meiosis-associated argonaute (MAGO) proteins are necessary for meiosis in maize

Project description:Plants do not specify their germline until late in their life cycle. Hence, the plant germline is normally specified from terminally differentiated somatic cells, though the precise mechanism(s) are unknown. We have found that male gametogenesis in maize is associated with the accumulation of distinct 21-nt phased small-interfering RNAs (phasiRNAs) generated by meiosis-associated argonaute (MAGO) proteins. MAGO1 accumulates in the epidermis of pre-meiotic anthers while MAGO2 is found in developing meiocytes. We have found that MAGO proteins are required for meiocyte development as mutants display chromosomal defects and male infertility. Furthermore, we detect the heat stress-induced activation of a distinct class of Long terminal repeat retrotransposons in the male germline of MAGO mutants. Our data suggests that MAGO proteins and the reproductive phasiRNAs play important roles protecting the germline from transposable elements during environmental stress conditions.

2022-01-04 | PXD013891 | Pride

ROR1 can interact with TCL1 and enhance leukemogenesis in E?-TCL1 transgenic mice.

Project description: Not available

| S-EPMC3896194 | biostudies-literature

ADAD2 regulates heterochromatin in meiotic and post-meiotic male germ cells via translation of MDC1

Project description:Male germ cells establish a unique heterochromatin domain, the XY-body, early in meiosis. How this domain is maintained through the end of meiosis and into post-meiotic germ cell differentiation is poorly understood. ADAD2 is a late meiotic male germ cell specific RNA binding protein, loss of which leads to post-meiotic germ cell defects. Analysis of ribosome association in Adad2 mutants revealed defective translation of Mdc1, a key regulator of XY-body formation, late in meiosis. As a result, Adad2 mutants show normal establishment but failed maintenance of the XY-body. Observed XY-body defects are concurrent with abnormal autosomal heterochromatin and ultimately lead to severely perturbed post-meiotic germ cell heterochromatin and cell death. These findings highlight the requirement of ADAD2 for Mdc1 translation, the role of MDC1 in maintaining meiotic male germ cell heterochromatin, and the importance of late meiotic heterochromatin for normal post-meiotic germ cell differentiation.

2021-12-11 | GSE190525 | GEO

Saccharomyces cerevisiae

Project description:Splicing defects in RNA export receptor mutants

| PRJNA360580 | ENA