Septin-dependent invasive growth by the rice blast fungus Magnaporthe oryzae

Septin GTPases are morphogenetic proteins that are widely conserved in eukaryotic organisms fulfilling diverse roles in cell division, differentiation and development. In the filamentous fungal pathogen Magnaporthe oryzae, the causal agent of the devastating blast diseases of rice and wheat, septins have been shown to be essential for plant infection. The blast fungus elaborates a specialised infection structure called an appressorium with which it mechanically ruptures the plant cuticle. Septin aggregation and generation of a hetero-oligomeric ring structure at the base of the infection cell is indispensable for plant infection. Furthermore, once the fungus enters host tissue it develops another infection structure, the transpressorium, enabling it to move between living host plant cells, which also requires septins for its function. Specific inhibition of septin aggregation—either genetically or with chemical inhibitors—prevents plant infection. Significantly, by screening for inhibitors of septin aggregation, broad spectrum anti-fungal compounds have been identified that prevent rice blast and a number of other cereal diseases in field trials. We review the recent advances in our understanding of septin biology and their potential as targets for crop disease control

The emerging role of septins in fungal pathogenesis

Fungal pathogens undergo specific morphogenetic transitions in order to breach the outer surfaces of plants and invade the underlying host tissue. The ability to change cell shape and switch between non-polarised and polarised growth habits is therefore critical to the lifestyle of plant pathogens. Infection-related development involves remodelling of the cytoskeleton, plasma membrane and cell wall at specific points during fungal pathogenesis. Septin GTPases are components of the cytoskeleton that play pivotal roles in actin remodelling, micron-scale plasma membrane curvature sensing and cell polarity. Septin assemblages, such as rings, collars and gauzes, are known to have important roles in cell shape changes and are implicated in formation of specialised infection structures to enter plant cells. Here, we review and compare the reported functions of septins of plant pathogenic fungi, with a special focus on invasive growth. Finally, we discuss septins as potential targets for broad-spectrum antifungal plant protection strategies

Using light scattering to assess how phospholipid-protein interactions affect complex I functionality in liposomes

Complex I is an essential membrane protein in respiration, oxidising NADH and reducing ubiquinone to contribute to the proton-motive force that powers ATP synthesis. Liposomes provide an attractive platform to investigate complex I in a phospholipid membrane with the native hydrophobic ubiquinone substrate and proton transport across the membrane, but without convoluting contributions from other proteins present in the native mitochondrial inner membrane. Here, we use dynamic and electrophoretic light scattering techniques (DLS and ELS) to show how physical parameters, in particular the zeta potential (ζ-potential), correlate strongly with the biochemical functionality of complex I-containing proteoliposomes. We find that cardiolipin plays a crucial role in the reconstitution and functioning of complex I and that, as a highly charged lipid, it acts as a sensitive reporter on the biochemical competence of proteoliposomes in ELS measurements. We show that the change in ζ-potential between liposomes and proteoliposomes correlates linearly with protein retention and catalytic oxidoreduction activity of complex I. These correlations are dependent on the presence of cardiolipin, but are otherwise independent of the liposome lipid composition. Moreover, changes in the ζ-potential are sensitive to the proton motive force established upon proton pumping by complex I, thereby constituting a complementary technique to established biochemical assays. ELS measurements may thus serve as a more widely useful tool to investigate membrane proteins in lipid systems, especially those that contain charged lipids

A new type of Halimeda bioherm on the Queensland Plateau, NE Australia

Morphology, internal structure, and in situ facies distribution of mesophotic Halimeda bioherms from the Queensland Plateau (NE Australia) are presented based on hydroacoustic and oceanographic data, seafloor observations, and discrete sediment sampling carried out during RV SONNE cruise SO292 in 2022. Halimeda buildups consist of cone-like mounds up to 500 m in diameter and 3–10 m high, with gentle slopes (2°–5° on the top of Tregrosse Bank). Bioherms occur in water depths of 10–70 m, with most bioherm between 50 and 65 m. Their internal structure consists of aggrading low-amplitude reflections at the core of the bioherm interfingering with high-amplitude reflections to the flanks. Surface facies distribution displays one to four facies belts, from distal to proximal: Halimeda rudstone, Halimeda rudstone with living plants, Halimeda rudstone with coralgal debris, and coralgal boundstone (when present, occupied the top of the bioherms). It is proposed that the alternation of two key processes contributes to the formation of these bioherms: (1) in situ accumulation of Halimeda debris and (2) episodic dismantling of the mesophotic coralgal boundstone at the centre of the bioherm by severe storms. These storms may dismantle the mesophotic reef and export coralgal rubble to the flanks. Flanks may be recolonized by Halimeda during fair-weather periods. Due to their different geomorphic expressions, complex internal structure, and surficial facies distribution, we suggest that the buildups of the Queensland Plateau represent a new Halimeda bioherm morphotype, distinct from previously described bioherms on the adjacent Great Barrier Reef and elsewhere globally.03G0292A—ICECARB from the Bundesministerium für Bildung und Forschung (Germany) to CBSpanish Ministry of Science and Innovation (MCIN) through the Ramón y Cajal Project RYC2021-034362-I (MCIN/ AEI/https:// doi. org/ 10. 13039/ 50110 00110 33 and NextGenerationEU/ PRTR)Parks Australia for the research permit for Cruise SO292 (permit EPBC 2022/9168)The Schmidt Ocean Institute is thanked for the RV Falkor multibeam data acquired during cruises FK200429 and FK200802

Poly (A) binding protein cytoplasmic 1 is a novel co-regulator of the androgen receptor

The androgen receptor (AR) is a member of the steroid receptor superfamily that regulates gene expression in a ligand-dependent manner. The NTD of the AR plays a key role in AR transactivation including androgen-independent activation of the AR in castration-resistant prostate cancer (CRPC) cells. We recently reported that amino acids (a.a.) 50-250 of the NTD are capable of modulating AR nucleocytoplasmic trafficking. To further explore the mechanism associated with a.a. 50-250, GFP pull-down assays were performed in C4-2 CRPC cells transfected with GFP tagged a.a. 50-250 of the AR. Mass spectrometry analysis of the pulled down proteins identified poly (A) binding protein cytoplasmic 1 (PABPC1) interaction with this region of the AR. In silicoanalysis of gene expression data revealed PABPC1 up-regulation in prostate cancer tissue specimens and this up-regulation correlates to increased disease recurrence. Co-immunoprecipitation assays confirmed the association of PABPC1 with a.a. 50-250 of the NTD of the AR. Knockdown of PABPC1 decreased nuclear AR protein levels and inhibited androgen activation of the AR target PSA in LNCaP and C4-2 cells. Additionally, knockdown of PABPC1 inhibited transactivation of the PSA promoter by NAR (AR lacking the LBD) and attenuated proliferation of AR-positive prostate cancer cells. These findings suggest that PABPC1 is a novel co-regulator of the AR and may be a potential target for blocking activation of the AR in CRPC

Androgen up-regulates vascular endothelial growth factor expression in prostate cancer cells via an Sp1 binding site

Background\ud Vascular Endothelial Growth Factor (VEGF) is regulated by a number of different factors, but the mechanism(s) behind androgen-mediated regulation of VEGF in prostate cancer are poorly understood.\ud \ud Results\ud Three novel androgen receptor (AR) binding sites were discovered in the VEGF promoter and in vivo binding of AR to these sites was demonstrated by chromatin immunoprecipitation. Mutation of these sites attenuated activation of the VEGF promoter by the androgen analog, R1881 in prostate cancer cells. The transcription factors AR and Sp1 were shown to form a nuclear complex and both bound the VEGF core promoter in chromatin of hormone treated CWR22Rv1 prostate cancer cells. The importance of the Sp1 binding site in hormone mediated activation of VEGF expression was demonstrated by site directed mutagenesis. Mutation of a critical Sp1 binding site (Sp1.4) in the VEGF core promoter region prevented activation by androgen. Similarly, suppression of Sp1 binding by Mithramycin A treatment significantly reduced VEGF expression.\ud \ud Conclusions\ud Our mechanistic study of androgen mediated induction of VEGF expression in prostate cancer cells revealed for the first time that this induction is mediated through the core promoter region and is dependent upon a critical Sp1 binding site. The importance of Sp1 binding suggests that therapy targeting the AR-Sp1 complex may dampen VEGF induced angiogenesis and, thereby, block prostate cancer progression, helping to maintain the indolent form of prostate cancer

Chia-Yang Chen, clarinet

Max RegerKrzysztof PendereckiPaul PierneRoberto SierraGeorge Gershwi

The appressorium at a glance

Many plant pathogenic fungi have the capacity to infect their plant hosts using specialised cells called appressoria. These structures act as a gateway between the fungus and host, allowing entry to internal tissues. Appressoria apply enormous physical force to rupture the plant surface, or use a battery of enzymes to digest the cuticle and plant cell wall. Appressoria also facilitate focal secretion of effectors at the point of plant infection to suppress plant immunity. These infection cells develop in response to the physical characteristics of the leaf surface, starvation stress and signals from the plant. Appressorium morphogenesis has been linked to septin-mediated reorganisation of F-actin and microtubule networks of the cytoskeleton, and remodelling of the fungal cell wall. In this Cell Science at a Glance and accompanying poster, we highlight recent advances in our understanding of the mechanisms of appressorium-mediated infection, and compare development on the leaf surface to the biology of invasive growth by pathogenic fungi. Finally, we outline key gaps in our current knowledge of appressorium cell biology