scholarly journals Glycosylation and immunocytochemistry of binucleate cells in pronghorn (Antilocapra americana, Antilocapridae) show features of both Giraffidae and Bovidae

Placenta ◽  
2017 ◽  
Vol 57 ◽  
pp. 216-222
Author(s):  
Carolyn J.P. Jones ◽  
W.J. Silvia ◽  
C.H. Hamilton ◽  
T.W. Geary ◽  
A.L. Zezeski ◽  
...  
Placenta ◽  
2017 ◽  
Vol 57 ◽  
pp. 312
Author(s):  
Carolyn Jones ◽  
W.J. Silvia (deceased) ◽  
C.H. Hamilton ◽  
T.W. Geary ◽  
Abigail Zezeski ◽  
...  

2005 ◽  
Vol 69 (4) ◽  
pp. 1463-1474 ◽  
Author(s):  
CATHERINE L. STEPHEN ◽  
DON G. WHITTAKER ◽  
DON GILLIS ◽  
LINDSEY L. COX ◽  
OLIN E. RHODES

1993 ◽  
Vol 104 (2) ◽  
pp. 227-230
Author(s):  
U. Kues ◽  
L.A. Casselton

Having multiple mating types greatly improves the chances of meeting a compatible mating partner, particularly in an organism like the mushroom that has no sexual differentiation and no mechanism for signalling to a likely mate. Having several thousands of mating types, as some mushrooms do, is, however, remarkable - and even more remarkable is the fact that individuals only recognise that they have met a compatible mate after their cells have fused. How are such large numbers of mating types generated and what is the nature of the intracellular interaction that distinguishes self from non- self? Answers to these fascinating questions come from cloning some of the mating type genes of the ink cap mushroom Coprinus cinereus. A successful mating in Coprinus triggers a major switch in cell type, the conversion of a sterile mycelium with uninucleate cells (monokaryon) to a fertile mycelium with binucleate cells (dikaryon) which differentiates the characteristic fruit bodies. The mating type genes that regulate this developmental switch map to two multiallelic loci designated A and B and these must both carry different alleles for full mating compatibility. A and B independently regulate different steps in the developmental switch, making it possible to study just one component of the system and work in our laboratory has concentrated on understanding the structure and function of the A genes. It is estimated that some 160 different A mating types exist in nature, any two of which can together trigger the A-regulated part of sexual development. The first clue to how such large numbers are generated came from classical genetic analysis, which identified two functionally redundant A loci, (alpha) and beta. Functional redundancy is, indeed, the key to multiple A mating types and, as seen in Fig.1, molecular cloning has identified many more genes than was possible by recombination analysis.


2000 ◽  
Vol 113 (7) ◽  
pp. 1223-1230 ◽  
Author(s):  
J. Liu ◽  
H. Wang ◽  
M.K. Balasubramanian

Cell division in Schizosaccharomyces pombe is achieved through the use of a medially positioned actomyosin ring. A division septum is formed centripetally, concomitant with actomyosin ring constriction. Genetic screens have identified mutations in a number of genes that affect actomyosin ring or septum assembly. These cytokinesis-defective mutants, however, undergo multiple S and M phases and die as elongated cells with multiple nuclei. Recently, we have shown that a mutant allele of the S. pombe drc1(+)/cps1(+) gene, which encodes a 1,3-(beta)-glucan synthase subunit, is defective in cytokinesis but displays a novel phenotype. drc1-191/cps1-191 cells are capable of assembling actomyosin rings and completing mitosis, but are incapable of assembling the division septum, causing them to arrest as binucleate cells with a stable actomyosin ring. Each nucleus in arrested cps1-191 cells is able to undergo S phase but these G(2) nuclei are significantly delayed for entry into the M phase. In this study we have investigated the mechanism that causes cps1-191 to block with two G(2) nuclei. We show that the inability of cps1-191 mutants to proceed through multiple mitotic cycles is not related to a defect in cell growth. Rather, the failure to complete some aspect of cytokinesis may prevent the G(2)/M transition of the two interphase-G(2) nuclei. The G(2)/M transition defect of cps1-191 mutants is suppressed by a mutation in the wee1 gene and also by the dominant cdc2 allele cdc2-1w, but not the cdc2-3w allele. Transient depolymerization of all F-actin structures also allowed a significant proportion of the cps1-191 cells to undergo a second round of mitosis. We conclude that an F-actin and Wee1p dependent checkpoint blocks G(2)/M transition until previous cytokinesis is completed.


2007 ◽  
Vol 7 ◽  
pp. 1008-1023 ◽  
Author(s):  
Tetsuji Nagata

In order to study the aging changes of intramitochondrial protein synthesis in mouse hepatocytes, 10 groups of aging mice, each consisting of three individuals, total 30, from fetal day 19 to postnatal year 2, were injected with3H-leucine, a protein precursor, sacrificed 1 h later, and the liver tissues processed for electron microscopic radioautography. On electron microscopic radioautograms obtained from each animal, the numbers of mitochondria, the numbers of labeled mitochondria, and the mitochondrial labeling index labeled with3H-leucine that showed protein synthesis in each hepatocyte, both mononucleate and binucleate cells, were counted and the averages in respective aging groups were compared. From the results, it was demonstrated that the numbers of mitochondria, the numbers of labeled mitochondria, and the labeling indices of intramitochondrial protein syntheses in both mononucleate and binucleate hepatocytes of mice at various ages increased due to development of animals. The numbers of mitochondria, the numbers of labeled mitochondria, and the labeling indices of intramitochondrial protein synthesis in binucleate hepatocytes were more than those of mononucleate hepatocytes at the same aging stages.


2009 ◽  
Vol 40 (4) ◽  
pp. 803-805 ◽  
Author(s):  
Khursheed R. Mama ◽  
Samantha Uhrig ◽  
David S. Miller ◽  
Lauren Harris ◽  
Melissa Syndergaard ◽  
...  

eLife ◽  
2016 ◽  
Vol 5 ◽  
Author(s):  
Jill Elaine Falk ◽  
Dai Tsuchiya ◽  
Jolien Verdaasdonk ◽  
Soni Lacefield ◽  
Kerry Bloom ◽  
...  

In budding yeast, if the spindle becomes mispositioned, cells prevent exit from mitosis by inhibiting the mitotic exit network (MEN). The MEN is a signaling cascade that localizes to spindle pole bodies (SPBs) and activates the phosphatase Cdc14. There are two competing models that explain MEN regulation by spindle position. In the 'zone model', exit from mitosis occurs when a MEN-bearing SPB enters the bud. The 'cMT-bud neck model' posits that cytoplasmic microtubule (cMT)-bud neck interactions prevent MEN activity. Here we find that 1) eliminating cMT– bud neck interactions does not trigger exit from mitosis and 2) loss of these interactions does not precede Cdc14 activation. Furthermore, using binucleate cells, we show that exit from mitosis occurs when one SPB enters the bud despite the presence of a mispositioned spindle. We conclude that exit from mitosis is triggered by a correctly positioned spindle rather than inhibited by improper spindle position.


2008 ◽  
Vol 211 (5) ◽  
pp. 749-756 ◽  
Author(s):  
J. Hebert ◽  
A. Lust ◽  
A. Fuller ◽  
S. K. Maloney ◽  
D. Mitchell ◽  
...  

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