In addition, the nucleotide sequence for the Nowa cDNA was shown with an incorrect GenBank accession number. The correct GenBank accession number is AF539862. AUTHOR CORRECTION IntroductionPattern formation within single cells has been recently recognized as a fundamental but not well understood aspect of cell biology (Shulman and St Johnston, 1999). A particularly fascinating example is the morphogenesis of the nematocyst, a complex structure that develops inside a giant secretory vesicle in the cnidarian nematocyte (Slautterback and Fawcett, 1959;Holstein, 1981). Upon stimulation of the nematocyte, the nematocyst discharges explosively, a process that takes less than 3 milliseconds (Holstein and Tardent, 1984).The basic structure of the nematocyst consists of a capsule with a double-layered wall, a matrix with an inverted tubule bearing spines, and an operculum. Based on this structure, a wide diversity of morphological types of nematocysts (Fig. 1A) has evolved that serve different functions such as capture of prey and defense (Mariscal, 1974;.Nematocyst morphogenesis can be subdivided into five stages (Holstein, 1981). (1) An early growth phase during which the capsule primordium forms and grows by addition of new vesicles to the vesicle harboring the capsule. (2) A late growth phase during which a tubule forms outside the capsule by addition of more vesicles; capsule and tubule wall form a continuous structure. (3) Invagination of the long external tubule into the capsule. (4) An early maturation phase leading to the formation of spines by condensation of the protein spinalin (Koch et al., 1998) inside the invaginated tubule. (5) A final late maturation step during which poly-γ-glutamate is synthesized in the matrix of the capsule. This generates an osmotic pressure of 150 bar that drives discharge (Weber, 1990;Szczepanek et al., 2002).The extremely high pressure in mature capsules requires high tensile strength of the wall. This tensile strength is mediated by minicollagens, a family of very short collagens that form the capsule's inner wall (Kurz et al., 1991;Holstein et al., 1994). In a previous paper (Engel et al., 2001), we have shown that wall maturation involves polymerization of minicollagens to an insoluble polymer. This polymerization is mediated by disulfides in the minicollagen cysteine-rich domains (MCCR domains) that undergo a switch from intrachain to inter-chain disulfide bonds in the late maturation phase. The inner wall layer, formed by minicollagens, is covered by an outer wall layer, which is more electron-dense than the inner wall in EM sections of nematocysts (Holstein, 1981;Watson and Mariscal, 1984) and appeared as a layer of globular material in field emission scanning electron microscopy (Holstein et al., 1994). The molecular nature of this outer wall was previously unknown.In this study we used the monoclonal antibody H22 (mAb H22) (Kurz et al., 1991), which stained the outer wall of Hydra nematocysts throughout morphogenesis and in mature readyto-discharge nematocysts in the tent...
Herpes simplex virus-1 (HSV-1) is a significant human pathogen. Upon infection, HSV-1 expresses its immediate early (IE) genes, and the IE transcription factor ICP4 (infectious cell protein-4) plays a pivotal role in initiating the downstream gene-expression cascade. Using live-cell time-lapse fluorescence microscopy, flow cytometry, qPCR, and chromatin immunoprecipitation, we quantitatively monitored the expression of ICP4 in individual cells after infection. We find that extrinsic stimuli can accelerate ICP4 kinetics without increasing ICP4 protein or mRNA levels. The accelerated ICP4 kinetics-despite unchanged steady-state ICP4 protein or mRNA level-correlate with increased HSV-1 replicative fitness. Hence, the kinetics of ICP4 functionally mirror the kinetics of the human herpesvirus cytomegalovirus IE2 "accelerator" circuit, indicating that IE accelerator circuitry is shared among the alpha and beta herpesviruses. We speculate that this circuit motif is a common evolutionary countermeasure to throttle IE expression and thereby minimize the inherent cytotoxicity of these obligate viral transactivators.
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