A cell that dies during wild-type C. elegans development can function as a neuron in a ced-3 mutant

Mutations in the C. elegans gene ced-3 prevent almost all programmed cell deaths, so that in a ced-3 mutant there are many extra cells. We show that the pharyngeal neuron M4 is essential for feeding in wild-type worms, but in a ced-3 mutant, one of the extra cells, probably MSpaaaaap (the sister of M4), can sometimes take over M4's function. The function of MSpaaaaap, unlike that of M4, is variable and subnormal. One possible explanation is that its fate, being hidden by death and not subject to selection, has drifted randomly during evolution. We suggest that such cells may play roles in the evolution of cell lineage analogous to those played by pseudogenes in the evolution of genomes.     

CED-2/CrkII and CED-10/Rac control phagocytosis and cell migration in Caenorhabditis elegans

Engulfment of apoptotic cells in Caenorhabditis elegans is controlled by two partially redundant pathways. Mutations in genes in one of these pathways, defined by the genes ced-2, ced-5 and ced-10, result in defects both in the engulfment of dying cells and in the migrations of the two distal tip cells of the developing gonad. Here we find that ced-2 and ced-10 encode proteins similar to the human adaptor protein CrkII and the human GTPase Rac, respectively. Together with the previous observation that ced-5 encodes a protein similar to human DOCK180, our findings define a signalling pathway that controls phagocytosis and cell migration. We provide evidence that CED-2 and CED-10 function in engulfing rather than dying cells to control the phagocytosis of cell corpses, that CED-2 and CED-5 physically interact, and that ced-10 probably functions downstream of ced-2 and ced-5. We propose that CED-2/CrkII and CED-5/DOCK180 function to activate CED-10/Rac in a GTPase signalling pathway that controls the polarized extension of cell surfaces.     

Fate of the nuclear lamina during Caenorhabditis elegans apoptosis

Invertebrates and in Drosophila, lamins and lamin-associated proteins are primary targets for cleavage by caspases. Eliminating mammalian lamins causes apoptosis, whereas expressing mutant lamins that cannot be cleaved by caspase-6 delay apoptosis. Caenorhabditis elegans has a single lamin protein, Ce-lamin, and a caspase, CED-3, that is responsible for most if not all somatic apoptosis. In this study we show that in C. elegans embryos induced to undergo apoptosis Ce-lamin is degraded surprisingly late. In such embryos CED-4 translocated to the nuclear envelope but the cytological localization of Ce-lamin remained similar to that in wild-type embryos. TUNEL labeling indicated that Ce-lamin was degraded only after DNA is fragmented. Ce-lamin, Ce-emerin, or Ce-MAN1 were not cleaved by recombinant CED-3, showing that these lamina proteins are not substrates for CED-3 cleavage. These results suggest that lamin cleavage probably is not essential for apoptosis in C. elegans.     

In vivo effects on intron retention and exon skipping by the U2AF large subunit and SF1/BBP in the nematode Caenorhabditis elegans

The in vivo analysis of the roles of splicing factors in regulating alternative splicing in animals remains a challenge. Using a microarray-based screen, we identified a Caenorhabditis elegans gene, tos-1, that exhibited three of the four major types of alternative splicing: intron retention, exon skipping, and, in the presence of U2AF large subunit mutations, the use of alternative 3' splice sites. Mutations in the splicing factors U2AF large subunit and SF1/BBP altered the splicing of tos-1. 3' splice sites of the retained intron or before the skipped exon regulate the splicing pattern of tos-1. Our study provides in vivo evidence that intron retention and exon skipping can be regulated largely by the identities of 3' splice sites.     

Control by bacteriophage T4 of two sequential phosphorylations of the alpha subunit of Escherichia coli RNA polymerase

The effect of 2′-O-methylation upon the base-stacking properties of dinucleoside monophosphates has been studied by circular dichroism measurements over the temperature range from ?20 °C to +80 °C at high and at low salt concentration of 13 2′-O-methyl derivatives in neutral aqueous solution. It is found that 2′-O methylation generally enhances the stacking propensity of dinucleoside monophosphates except for the dimers with adenine in the 3′-linked nucleoside, where the converse trend is observed. The influence of 2′-O-methylation upon the base-stacking property of a dimer correlates in part with the effect of a reduction in salt concentration, suggesting that the 2′-O-methyl group effects the stacking by displacing ions from the immediate environment of the dimer as well as by intramolecular steric effects. The dimers which exhibit an enhanced stacking due to the 2′-O-methylation are found in a larger than statistical abundance in yeast transfer RNA, whereas those showing a reduced stacking occur in minor abundance. These observations are discussed in relation to some current views on the role of modified nucleosides in the conformation of ribonucleic acids.     

Analysis of how ant behaviors affect germination in a tropical myrmecochore Calathea microcephala (P. & E.) Koernicke (Marantaceae): Microsite selection and aril removal by neotropical ants,Odontomachus, Pachycondyla,and Solenopsis (Formicidae)

Summary The evolutionary effects of a tropical ant-seed interaction are examined by posing questions about the fate of Calathea seeds carried by neotropical ants. Where do ants take seeds and what do they do with them? How do ant behaviors affect seed germination? Treatment of seeds by ants is determined by a series of seed-fate trials in captive colonies. There is no evidence of seed predation by ants. Odontomachus laticeps, Pachycondyla spp, and Solenopsis geminata rapidly displace seeds to ant nests, determine the microsites of seeds, and remove the seed arils for food. The seed arils are rich in lipids. The effects on germination of microsite selection and aril removal are quantitatively evaluated. Seeds which are immediately taken to a consistently moist spot germinate readily; 72% germinate, with a mean germination speed of 29 days. For such seeds aril removal does not significantly affect germination. In contrast, seeds which experience a delay before encountering appropriate germination conditions seem to exhibit an induced dormancy (sensu, Harper 1977) and a lower germination percentage. They take longer to germinate (up to 85 days) even after conditions become appropriate. It appears that their germination is enhanced by aril removal, which may act as an environmental cue to break dormancy. Such a mechanism would indicate that ant-handling of seeds is predictive of favorable conditions for seedling growth and establishment. The exact nature of such conditions and the effects on plant population dynamics remain to be seen.     

lin-17 mutations of Caenorhabditis elegans disrupt certain asymmetric cell divisions

The identification of a gene necessary for the asymmetry of cell division would be an important first step toward understanding how sister cells come to differ in their developmental fates. The lin-17 gene of the nematode Caenorhabditis elegans is an excellent candidate for being such a gene. lin-17 mutations cause several blast cells that normally generate sister cells of two distinct types to generate instead sister cells of the same type. Moreover, lin-17 mutations cause sister cells to be equal in size as well as equivalent in developmental fate, suggesting that lin-17 acts at or prior to the asymmetric cell division. The lin-17 gene product is involved in asymmetric cell divisions in a variety of tissues, indicating that lin-17 functions in a general mechanism for the establishment of cellular asymmetry in parent cells.     

Genbank accession #: AF 124983

Plant Molecular Biology -     

A Visible Allele of the Muscle Gene sup-10 X of C. ELEGANS

In this paper, we extend our previous analyses of a set of genes in Caenorhabditis elegans that are involved in muscle structure and function: unc-93 III, sup-9 II, sup-10 X and sup-11 I. We describe an unusual, visible allele of sup-10, examine how this allele interacts genetically with mutations in other genes of this set and propose that the wild-type products of the unc-93 and sup-10 loci may be components of a protein complex. We also describe a new gene of this set, sup-18 III, and the interaction of sup-18 alleles with mutations in the other genes.