Control of plasma membrane-associated actin polymerization specifies the pattern of the cell wall in xylem vessels.
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1207997 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR31929740.fastq.gz | Fastqsanger.gz | |||
| SRR31929741.fastq.gz | Fastqsanger.gz | |||
| SRR31929742.fastq.gz | Fastqsanger.gz | |||
| SRR31929743.fastq.gz | Fastqsanger.gz | |||
| SRR31929744.fastq.gz | Fastqsanger.gz |
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Project description:Cell wall patterning is central to determining the shape and function of plant cells. Protoxylem and metaxylem vessel cells deposit banded and pitted cell walls, respectively, which enable their distinctive water transport capabilities, but the mechanisms that specify which cell wall pattern is laid down remain unknown. Here, we show that the pitted cell wall pattern in metaxylem vessels is specified by transcriptional control of actin polymerization. A newly isolated allele of KNOTTED-like homeobox transcription factor 7 (KNAT7) was associated with the formation of banded cell walls in metaxylem vessels. To identify the genes responsible for altering the cell wall pattern in knat7 xylem vessels, we performed an RNA-seq analysis of knat7. We used in vitro cultures of hypocotyls and cotyledons because the population of differentiating xylem cells in intact roots is tiny and these methods efficiently induce ectopic differentiation of xylem vessel elements. Formin Homology Domain-Containing Protein 11 (FH11) was upregulated in knat7 metaxylem, but expressed only in protoxylem vessels in wild-type plants. Loss of FH11 suppressed the knat7 phenotype. Conversely, ectopic overexpression of FH11 in metaxylems mimicked the knat7 phenotype. FH11 function required its plasma membrane anchoring and the actin polymerization activity. Actin polymerization by FH11 at the plasma membrane caused the dispersion of activated ROP GTPases, the determinant of pit formation. These results suggest that decontrol of actin polymerization at the plasma membrane abolishes the pitted cell wall formation and promotes the formation of banded cell walls in metaxylem vessels. This study unveils the importance of the proper control of actin polymerization on cell wall pattern specification.
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Project description:Cell wall patterning is central to determining the shape and function of plant cells. Protoxylem and metaxylem vessel cells deposit banded and pitted cell walls, respectively, which enable their distinctive water transport capabilities. Here, we show that the pitted cell wall pattern in metaxylem vessels is specified by transcriptional control of actin polymerization. A newly isolated allele of KNOTTED-LIKE HOMEOBOX TRANSCRIPTION FACTOR 7 (KNAT7) was associated with the formation of banded cell walls in metaxylem vessels. Loss of KNAT7 caused misexpression of FORMIN HOMOLOGY DOMAIN CONTAINING PROTEIN11 (FH11) in the metaxylem, which in turn caused rearrangements of ROP GTPases and microtubules in banded patterns. FH11 function required its plasma membrane anchoring and actin polymerization activity. These results suggest that excessive actin polymerization at the plasma membrane abolishes the pitted cell wall formation and promotes banded cell wall formation in metaxylem vessels. This study unveils the importance of proper control of actin polymerization for cell wall pattern determination.
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Project description:Patterned cell wall deposition is crucial for cell shapes and functions. In Arabidopsis xylem vessels, ROP11 GTPase locally inhibits cell wall deposition through microtubule disassembly, inducing pits in cell walls. Here, we show that an additional ROP signaling pathway promotes cell wall growth at pit boundaries. Two proteins, Boundary of ROP domain1 (BDR1) and Wallin (WAL), localize to pit boundaries and regulate cell wall growth. WAL interacts with F-actin and promotes actin assembly at pit boundaries while BDR1 is a ROP effector. BDR1 interacts with WAL, suggesting that WAL could be recruited to the plasma membrane by a ROP-dependent mechanism. These results demonstrate that BDR1 and WAL mediate a ROP-actin pathway that shapes pit boundaries. The study reveals a distinct machinery in which two closely associated ROP pathways oppositely regulate cell wall deposition patterns for the establishment of tiny but highly specialized cell wall domains.
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Project description:Megakaryoblastic leukemia 1 (MKL1) promotes the regulation of essential cell processes, including actin cytoskeletal dynamics by co-activating serum response factor. Recently, the first human case with MKL1 deficiency, leading to a novel primary immunodeficiency, was identified. We report a second family with two siblings with a homozygous frameshift mutation in MKL1. The index case deceased as an infant from progressive and severe pneumonia by Pseudomonas aeruginosa and poor wound healing. The younger sib was preemptively transplanted shortly after birth. The immunodeficiency was marked by a pronounced actin polymerization defect and a strongly reduced motility and chemotactic response by MKL1-deficient neutrophils. Apart from the lack of MKL1, subsequent proteomic and transcriptomic analyses of patient neutrophils revealed actin and several actin-related proteins to be downregulated, confirming a role for MKL1 as transcriptional co-regulator. Degranulation was enhanced upon suboptimal neutrophil activation, while production of reactive oxygen species was normal. Neutrophil adhesion was intact but without proper spreading. The latter could explain the observed failure in firm adherence and transendothelial migration under flow conditions. No apparent defect in phagocytosis and bacterial killing was found. Also monocyte-derived macrophages showed intact phagocytosis; lymphocyte counts and proliferative capacity were normal. Non-hematopoietic primary patient fibroblasts demonstrated defective differentiation into myofibroblasts but normal migration and filamentous actin (F-actin) content, most probably due to compensatory mechanisms of MKL2, which is not expressed in neutrophils. Our findings extend current insight into the severe immune dysfunction in MKL1 deficiency, with cytoskeletal dysfunction and defective extravasation of neutrophils as most prominent features.
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Project description:The mechanisms underlying cancer metastasis remain poorly understood. Here, we report that TFAM deficiency rapidly and stably induced spontaneous lung metastasis in mice with liver cancer. Interestingly, unexpected polymerization of nuclear actin was observed in TFAM-knockdown HCC cells when cytoskeleton was examined. Polymerization of nuclear actin is causally linked to the high-metastatic ability of HCC cells by modulating chromatin accessibility and coordinating the expression of genes associated with extracellular matrix remodeling, angiogenesis, and cell migration. Mechanistically, TFAM deficiency blocked the TCA cycle and increased the intracellular malonyl-CoA levels. Malonylation of mDia2, which drives actin assembly, promotes its nuclear translocation. Importantly, inhibition of malonyl-CoA production or nuclear actin polymerization significantly impeded the spread of HCC cells in mice. Moreover, TFAM was significantly downregulated in metastatic HCC tissues and was associated with overall survival and time to tumor recurrence of HCC patients. Taken together, our study connects mitochondria to the metastasis of human cancer via uncovered mitochondria-to-nucleus retrograde signaling, indicating that TFAM may serve as an effective target to block HCC metastasis.
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