scholarly journals A transcriptomics resource reveals a transcriptional transition during ordered sarcomere morphogenesis in flight muscle

eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Maria L Spletter ◽  
Christiane Barz ◽  
Assa Yeroslaviz ◽  
Xu Zhang ◽  
Sandra B Lemke ◽  
...  
Keyword(s):  
Expression Profile ◽  
Heart Development ◽  
Transcriptional Control ◽  
Flight Muscle ◽  
Transcriptional Regulator ◽  
Knock Down ◽  
Vertebrate Muscle ◽  
Efficient Induction ◽  
Flight Muscles ◽  
Stretch Sensitivity

Muscles organise pseudo-crystalline arrays of actin, myosin and titin filaments to build force-producing sarcomeres. To study sarcomerogenesis, we have generated a transcriptomics resource of developing Drosophila flight muscles and identified 40 distinct expression profile clusters. Strikingly, most sarcomeric components group in two clusters, which are strongly induced after all myofibrils have been assembled, indicating a transcriptional transition during myofibrillogenesis. Following myofibril assembly, many short sarcomeres are added to each myofibril. Subsequently, all sarcomeres mature, reaching 1.5 µm diameter and 3.2 µm length and acquiring stretch-sensitivity. The efficient induction of the transcriptional transition during myofibrillogenesis, including the transcriptional boost of sarcomeric components, requires in part the transcriptional regulator Spalt major. As a consequence of Spalt knock-down, sarcomere maturation is defective and fibers fail to gain stretch-sensitivity. Together, this defines an ordered sarcomere morphogenesis process under precise transcriptional control – a concept that may also apply to vertebrate muscle or heart development.

scholarly journals Systematic transcriptomics reveals a biphasic mode of sarcomere morphogenesis in flight muscles regulated by Spalt

2017 ◽  
Author(s):  
Maria L. Spletter ◽  
Christiane Barz ◽  
Assa Yeroslaviz ◽  
Xu Zhang ◽  
Sandra B. Lemke ◽  
...  
Keyword(s):  
Heart Development ◽  
Transcriptome Sequencing ◽  
Morphological Analysis ◽  
Flight Muscle ◽  
Transcriptional Regulator ◽  
Temporal Gene Expression ◽  
Vertebrate Muscle ◽  
Flight Muscles ◽  
Formation Phase ◽  
Stretch Sensitivity

AbstractMuscles organise pseudo-crystalline arrays of actin, myosin and titin filaments to build force-producing sarcomeres. To study how sarcomeres are built, we performed transcriptome sequencing of developing Drosophila flight muscles and identified 40 distinct expression profile clusters. Strikingly, two clusters are strongly enriched for sarcomeric components. Temporal gene expression together with detailed morphological analysis enabled us to define two distinct phases of sarcomere development, which both require the transcriptional regulator Spalt major. During the sarcomere formation phase, 1.8 μm long immature sarcomeres assemble myofibrils that spontaneously contract. During the sarcomere maturation phase, these sarcomeres grow to their final 3.2 μm length and 1.5 μm diameter and acquire stretch-sensitivity. Interestingly, the final number of myofibrils per flight muscle fiber is determined at the onset of the first phase. Together, this defines a biphasic mode of sarcomere and myofibril morphogenesis – a new concept that may also apply to vertebrate muscle or heart development.

scholarly journals Chromatin-Directed Proteomics Identifies ZNF84 as a p53-Independent Regulator of p21 in Genotoxic Stress Response

Cancers ◽  
2021 ◽  
Vol 13 (9) ◽  
pp. 2115
Author(s):  
Anna Strzeszewska-Potyrała ◽  
Karolina Staniak ◽  
Joanna Czarnecka-Herok ◽  
Mahmoud-Reza Rafiee ◽  
Marcin Herok ◽  
...  
Keyword(s):  
Transcriptional Control ◽  
Genotoxic Stress ◽  
Vital Role ◽  
Dna Double Strand Breaks ◽  
Independent Manner ◽  
Strand Breaks ◽  
Knock Down ◽  
Proteomic Approach ◽  
Gene And Protein Expression ◽  
Transcriptomic Changes

The p21WAF1/Cip1 protein, encoded by CDKN1A, plays a vital role in senescence, and its transcriptional control by the tumour suppressor p53 is well-established. However, p21 can also be regulated in a p53-independent manner, by mechanisms that still remain less understood. We aimed to expand the knowledge about p53-independent senescence by looking for novel players involved in CDKN1A regulation. We used a chromatin-directed proteomic approach and identified ZNF84 as a novel regulator of p21 in various p53-deficient cell lines treated with cytostatic dose of doxorubicin. Knock-down of ZNF84, an as-yet un-characterized protein, inhibited p21 gene and protein expression in response to doxorubicin, it attenuated senescence and was associated with enhanced proliferation, indicating that ZNF84-deficiency can favor senescence bypass. ZNF84 deficiency was also associated with transcriptomic changes in genes governing various cancer-relevant processes e.g., mitosis. In cells with ZNF84 knock-down we discovered significantly lower level of H2AX Ser139 phosphorylation (γH2AX), which is triggered by DNA double strand breaks. Intriguingly, we observed a reverse correlation between the level of ZNF84 expression and survival rate of colon cancer patients. In conclusion, ZNF84, whose function was previously not recognized, was identified here as a critical p53-independent regulator of senescence, opening possibilities for its targeting in novel therapies of p53-null cancers.

scholarly journals SEMA6D Expression and Patient Survival in Breast Invasive Carcinoma

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Dongquan Chen ◽  
Yufeng Li ◽  
Lizhong Wang ◽  
Kai Jiao
Keyword(s):  
Breast Cancer ◽  
Expression Profile ◽  
Heart Development ◽  
Invasive Carcinoma ◽  
Patient Survival ◽  
The Cancer Genome Atlas ◽  
Breast Cancer Patients ◽  
Genomic Expression ◽  
Cancer Genome Atlas ◽  
Public Datasets

Breast cancer (BC) is the second most common cancer diagnosed in American women and is also the second leading cause of cancer death in women. Research has focused heavily on BC metastasis. Multiple signaling pathways have been implicated in regulating BC metastasis. Our knowledge of regulation of BC metastasis is, however, far from complete. Identification of new factors during metastasis is an essential step towards future therapy. Our labs have focused on Semaphorin 6D (SEMA6D), which was implicated in immune responses, heart development, and neurogenesis. It will be interesting to know SEMA6D-related genomic expression profile and its implications in clinical outcome. In this study, we examined the public datasets of breast invasive carcinoma from The Cancer Genome Atlas (TCGA). We analyzed the expression of SEMA6D along with its related genes, their functions, pathways, and potential as copredictors for BC patients’ survival. We found 6-gene expression profile that can be used as such predictors. Our study provides evidences for the first time that breast invasive carcinoma may contain a subtype based on SEMA6D expression. The expression of SEMA6D gene may play an important role in promoting patient survival, especially among triple negative breast cancer patients.

scholarly journals Characterization of components of Z-bands in the fibrillar flight muscle of Drosophila melanogaster.

1989 ◽  
Vol 109 (5) ◽  
pp. 2157-2167 ◽  
Author(s):  
J D Saide ◽  
S Chin-Bow ◽  
J Hogan-Sheldon ◽  
L Busquets-Turner ◽  
J O Vigoreaux ◽  
...  
Keyword(s):  
Drosophila Melanogaster ◽  
Monoclonal Antibodies ◽  
Flight Muscle ◽  
Cross Reactivity ◽  
Antigenic Determinants ◽  
Immunogold Staining ◽  
Thick Filaments ◽  
The Matrix ◽  
Flight Muscles

Twelve monoclonal antibodies have been raised against proteins in preparations of Z-disks isolated from Drosophila melanogaster flight muscle. The monoclonal antibodies that recognized Z-band components were identified by immunofluorescence microscopy of flight muscle myofibrils. These antibodies have identified three Z-disk antigens on immunoblots of myofibrillar proteins. Monoclonal antibodies alpha:1-4 recognize a 90-100-kD protein which we identify as alpha-actinin on the basis of cross-reactivity with antibodies raised against honeybee and vertebrate alpha-actinins. Monoclonal antibodies P:1-4 bind to the high molecular mass protein, projectin, a component of connecting filaments that link the ends of thick filaments to the Z-band in insect asynchronous flight muscles. The anti-projectin antibodies also stain synchronous muscle, but, surprisingly, the epitopes here are within the A-bands, not between the A- and Z-bands, as in flight muscle. Monoclonal antibodies Z(210):1-4 recognize a 210-kD protein that has not been previously shown to be a Z-band structural component. A fourth antigen, resolved as a doublet (approximately 400/600 kD) on immunoblots of Drosophila fibrillar proteins, is detected by a cross reacting antibody, Z(400):2, raised against a protein in isolated honeybee Z-disks. On Lowicryl sections of asynchronous flight muscle, indirect immunogold staining has localized alpha-actinin and the 210-kD protein throughout the matrix of the Z-band, projectin between the Z- and A-bands, and the 400/600-kD components at the I-band/Z-band junction. Drosophila alpha-actinin, projectin, and the 400/600-kD components share some antigenic determinants with corresponding honeybee proteins, but no honeybee protein interacts with any of the Z(210) antibodies.

scholarly journals The Hippo pathway controls myofibril assembly and muscle fiber growth by regulating sarcomeric gene expression

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Aynur Kaya-Çopur ◽  
Fabio Marchiano ◽  
Marco Y Hein ◽  
Daniel Alpern ◽  
Julie Russeil ◽  
...  
Keyword(s):  
Gene Expression ◽  
Muscle Fiber ◽  
Flight Muscle ◽  
Hippo Pathway ◽  
Muscle Fibers ◽  
Muscle Growth ◽  
Fiber Growth ◽  
Flight Muscles ◽  
Sarcomeric Gene ◽  
The Hippo Pathway

Skeletal muscles are composed of gigantic cells called muscle fibers, packed with force-producing myofibrils. During development the size of individual muscle fibers must dramatically enlarge to match with skeletal growth. How muscle growth is coordinated with growth of the contractile apparatus is not understood. Here, we use the large Drosophila flight muscles to mechanistically decipher how muscle fiber growth is controlled. We find that regulated activity of core members of the Hippo pathway is required to support flight muscle growth. Interestingly, we identify Dlg5 and Slmap as regulators of the STRIPAK phosphatase, which negatively regulates Hippo to enable post-mitotic muscle growth. Mechanistically, we show that the Hippo pathway controls timing and levels of sarcomeric gene expression during development and thus regulates the key components that physically mediate muscle growth. Since Dlg5, STRIPAK and the Hippo pathway are conserved a similar mechanism may contribute to muscle or cardiomyocyte growth in humans.

Flight muscle and flight activity of melon fly, Bactrocera cucurbitae (Diptera: Tephritidae)

2021 ◽  
Vol 30 (2) ◽  
pp. 179-185
Author(s):  
Farhana Ferdousi ◽  
Shanjida Sultana ◽  
Tangin Akter ◽  
Pinakshi Roy ◽  
Shefali Begum
Keyword(s):  
Longitudinal Muscle ◽  
Flight Muscle ◽  
Flight Activity ◽  
The Other ◽  
Bactrocera Cucurbitae ◽  
Male And Female ◽  
Melon Fly ◽  
Length Width ◽  
Flight Muscles ◽  
The Mean

The flight activity and flight muscle of the melon fly, Bactrocera cucurbitae (Coquillett) (Diptera: Tephritidae) were observed. The Tethered technique was used to observe the flight activity in this study. The flight activity, and wing and flight muscles were compared between male and female melon flies. The results indicate that the female was relatively better and strong flier than the male. The mean duration of the flight activity of the females was 13.90 min/hour and of the males was 7.12 min./hour. The mean length, width, volume of wings of the males were 6.07 mm, 2.67 mm and 10.99 mm³, respectively. On the other hand, the mean length, width and volume of the wings of females were 7.07 mm, 2.87 mm and 15.60 mm³, respectively. In case of wing muscles, the mean volume of dorsal longitudinal muscle (DLM) in male and female was found 5.20 mm³ and 5.67 mm³, respectively. The mean length of flight wing muscle of male and female was 2.22 and 2.23 mm, respectively and the mean breadth of male and female was 1.65 and 1.77 mm, respectively. Dhaka Univ. J. Biol. Sci. 30(2): 179-185, 2021 (July)

Abstract 1422: Candesartan-induced Upregulation Of Transcriptional Regulator Yin Yang 1 Blocks Leukocyte-endothelial Interaction Under Physiological Flow.

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Hideto Ishii ◽  
Daisuke Mori ◽  
Mayuko Sato ◽  
Masayuki Yoshida
Keyword(s):  
Transcriptional Control ◽  
Recombinant Adenovirus ◽  
Recent Observation ◽  
Umbilical Vein ◽  
Dominant Role ◽  
Transcriptional Regulator ◽  
Potential Contribution ◽  
Flow Conditions ◽  
Yin Yang 1 ◽  
Yin Yang

[Objective] Transcriptional control of inflammation-relevant genes plays an important role in atherosclerosis. We have reported a dominant role of Yin Yang 1 (YY1), a transcriptional regulator, in proliferation of vascular smooth muscle cells (Santiago FS, Ishii H, et al. Circ Res in press). However, its effect in vascular endothelium remains unclear. Recent observation points a novel “genomic” effect of Angiotensin II to influence inflammation. In this study, we examined a potential contribution of YY1 in angiotensin type II receptor blocker (ARB)-mediated modulation of leukocyte-endothelial adhesion under flow condition. [Methods and Results] Human umbilical vein endothelial cells (HUVEC) were co-incubated in the presence or absence of candesartan, an ARB (1 uM) for 4 hours with TNFα (5 ng/ml). Treatment with candesartan dramatically inhibited THP-1 cell adhesion to TNFα-activated HUVEC under static (p <0.01) and flow conditions (p <0.05). We documented that upregulation of YY1 mRNA after candesartan treatment. To examine a role for YY1 in leukocyte-endothelial interaction, YY1 was overexpressed via recombinant adenovirus. The expression levels of VCAM-1 was significantly decreased in HUVEC treated with adenovirus YY1. In addition, adenovirus YY1 blocked THP-1 adhesion to TNFα-activated HUVEC under flow conditions (TNFα, 8.40±0.64/HPF; TNFα+candesartan, 1.93±0.54/HPF; p <0.0001). The expression level of phosphorylated-JNK, as determined by western blotting analysis, was reduced following YY1 transfection. In contrast, YY1 inhibition by YY1 siRNA did not influence leukocyte-endothelial adhesion and the expression of adhesion molecules. [Conclusion] We demonstrated that candesartan treatment upregulated YY1 in HUVEC and inhibited leukocyte-endothelial adhesion by inhibition of VCAM-1 expression. Our findings suggest a novel anti-inflammatory effect of ARB via YY1-dependent mechanisms.

Transcriptional regulation of cytoskeletal functions and segmentation by a novel maternal pair-rule gene, lilliputian

Development ◽  
2001 ◽  
Vol 128 (5) ◽  
pp. 801-813 ◽  
Author(s):  
A.H. Tang ◽  
T.P. Neufeld ◽  
G.M. Rubin ◽  
H.A. Muller
Keyword(s):  
Transcriptional Control ◽  
Fragile X ◽  
Transcriptional Regulator ◽  
Regulator Gene ◽  
Embryonic Patterning ◽  
Fushi Tarazu ◽  
Fragile X Mental Retardation ◽  
Pair Rule Gene ◽  
Mutant Phenotypes ◽  
Pair Rule

Transcriptional control during early Drosophila development is governed by maternal and zygotic factors. We have identified a novel maternal transcriptional regulator gene, lilliputian (lilli), which contains an HMG1 (AT-hook) motif and a domain with similarity to the human fragile X mental retardation FMR2 protein and the AF4 proto-oncoprotein. Embryos lacking maternal lilli expression show specific defects in the establishment of a functional cytoskeleton during cellularization, and exhibit a pair-rule segmentation phenotype. These mutant phenotypes correlate with markedly reduced expression of the early zygotic genes serendipity alpha, fushi tarazu and huckebein, which are essential for cellularization and embryonic patterning. In addition, loss of lilli in adult photoreceptor and bristle cells results in a significant decrease in cell size. Our results indicate that lilli represents a novel pair-rule gene that acts in cytoskeleton regulation, segmentation and morphogenesis.

scholarly journals Flight muscles degenerate by programmed cell death after migration in the wheat aphid, Sitobion avenae

2019 ◽  
Vol 12 (1) ◽  
Author(s):  
Honglin Feng ◽  
Xiao Guo ◽  
Hongyan Sun ◽  
Shuai Zhang ◽  
Jinghui Xi ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Molecular Mechanism ◽  
Differentially Expressed Genes ◽  
Flight Muscle ◽  
Sitobion Avenae ◽  
Differentially Expressed ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Muscle Degeneration ◽  
Flight Muscles

Abstract Objective Previous studies showed that flight muscles degenerate after migration in some aphid species; however, the underlying molecular mechanism remains virtually unknown. In this study, using the wheat aphid, Sitobion avenae, we aim to investigate aphid flight muscle degeneration and the underlying molecular mechanism. Results Sitobion avenae started to differentiate winged or wingless morphs at the second instar, the winged aphids were fully determined at the third instar, and their wings were fully developed at the fourth instar. After migration, the aphid flight muscles degenerated via programmed cell death, which is evidenced by a Terminal deoxynucleotidyl transferase dUTP-biotin nick-end labeling assay. Then, we identified a list of differentially expressed genes before and after tethered flights using differential-display reverse transcription-PCR. One of the differentially expressed genes, ubiquitin-ribosomal S27a, was confirmed using qPCR. Ubiquitin-ribosomal S27a is drastically up regulated following the aphids’ migration and before the flight muscle degeneration. Our data suggested that aphid flight muscles degenerate after migration. During flight muscle degeneration, endogenous proteins may be degraded to reallocate energy for reproduction.

scholarly journals Flying High—Muscle-Specific Underreplication in Drosophila

Genes ◽  
2020 ◽  
Vol 11 (3) ◽  
pp. 246 ◽  
Author(s):  
J. Spencer Johnston ◽  
Mary E. Zapalac ◽  
Carl E. Hjelmen
Keyword(s):  
Flow Cytometry ◽  
Dna Synthesis ◽  
Salivary Glands ◽  
Genome Size ◽  
Flight Muscle ◽  
S Phase ◽  
The Other ◽  
Tissue Type ◽  
Flight Muscles ◽  
Longitudinal Muscles

Drosophila underreplicate the DNA of thoracic nuclei, stalling during S phase at a point that is proportional to the total genome size in each species. In polytene tissues, such as the Drosophila salivary glands, all of the nuclei initiate multiple rounds of DNA synthesis and underreplicate. Yet, only half of the nuclei isolated from the thorax stall; the other half do not initiate S phase. Our question was, why half? To address this question, we use flow cytometry to compare underreplication phenotypes between thoracic tissues. When individual thoracic tissues are dissected and the proportion of stalled DNA synthesis is scored in each tissue type, we find that underreplication occurs in the indirect flight muscle, with the majority of underreplicated nuclei in the dorsal longitudinal muscles (DLM). Half of the DNA in the DLM nuclei stall at S phase between the unreplicated G0 and fully replicated G1. The dorsal ventral flight muscle provides the other source of underreplication, and yet, there, the replication stall point is earlier (less DNA replicated), and the endocycle is initiated. The differences in underreplication and ploidy in the indirect flight muscles provide a new tool to study heterochromatin, underreplication and endocycle control.

Sign in / Sign up

Export Citation Format

Share Document