Suction feeding fish differ in their capacity to generate subambient pressure while feeding, and these differences appear to relate to morphological variation. We developed a morphological model of force transmission in the fish head and parameterized it with measurements from individual fish. The model was applied to 45 individuals from five species of centrarchid fishes: Lepomis macrochirus, Lepomis punctatus, Lepomis microlophus, Micropterus salmoides and Pomoxis nigromaculatus. Measurements of epaxial cross-sectional area, epaxial moment arm, buccal area and buccal area moment arm were combined to estimate pressure generation capacity for individual fish. This estimation was correlated with pressure measured in fish feeding on elusive prey to test the model's ability to predict pressure generation from morphology. The model explained differences in pressure generation found among individuals (P<0.001, r 2 =0.71) and produced a realistic estimate of normalized muscle stress during suction feeding (68.5±6.7·kPa). Fish with smaller mouths, larger epaxial cross-sectional area and longer epaxial moments, such as L. macrochirus (bluegill sunfish), generated lower pressures than fish with larger mouths, smaller cross-sectional area and shorter moments, such as M. salmoides (largemouth bass). These results reveal a direct trade-off between morphological requirements of feeding on larger prey (larger mouth size relative to body depth) and the ability to generate subambient pressure while suction feeding on elusive prey.

Lymphoid and myeloid cells represent distinct lineages of a common hematopoietic stem cell (1-3). This distinction is dramatically illustrated in the autosomal recessive mouse mutant, scid . t Mice homozygous for the scid mutation (scid mice) are severely deficient in B and T lymphocytes whereas other hematopoietic cell types such as erythrocytes, monocytes, granulocytes, and megakaryocytes (all members of the myeloid series) are present in normal number (4, 5). Although the scid mutation appears to affect only lymphocyte development (4-10), it is not yet clear what stage of lymphoid differentiation is impaired or arrested .Recent results suggest that the effects of the scid mutation become manifest after the commitment of lymphoid cells to the B and T cell pathways . First, early transcription of unrearranged H chain and TCR loci, which presumably signals the opening of these loci to factors responsible for gene recombination (11-16), is detectable in scid fetal liver and thymus, respectively (Schuler, W., A. Schuler, and M. J. Bosma, unpublished results) . Second, although cells with H chain (or TCR) gene rearrangements cannot be directly demonstrated in freshly harvested lymphoid tissues of adult scid mice (17), early B cell lines with H chain gene rearrangements can be recovered from Abelson murine leukemia virus-transformed scid bone marrow cells (17) and from long-term cultures of scid bone marrow cells (18). There is also indication of early T cell development as thymic lymphomas with rearranged TCR-'Y and TCR-# alleles spontaneously appear in -15% of scid mice (5,17,19). It is striking, however, that the majority of rearranged H chain and TCR alleles in transformed scid lymphocytes show abnormal J region deletions. The deletions remove all J-coding exons of a given J region and appear to result from attempted D to J or V to Jjoining; they vary in size and extend both 5' and 3' of the deleted J regions (17,19). Evidence of abnormal J-associated deletions has also been reported for rearranged H chain alleles of long-term B cell lines derived from scid bone marrow cells (18).To explain the abnormal J-associated deletions and how they might account

Despite almost 50 years of research on the functional morphology and biomechanics of suction feeding, no consensus has emerged on how to characterize suction-feeding performance, or its morphological basis. We argue that this lack of unity in the literature is due to an unusually indirect and complex linkage between the muscle contractions that power suction feeding, the skeletal movements that underlie buccal expansion, the sharp drop in buccal suction pressure that occurs during expansion, the flow of water that enters the mouth to eliminate the pressure gradient, and the forces that are ultimately exerted on the prey by this flow. This complexity has led various researchers to focus individually on suction pressure, flow velocity, or the distance the prey moves as metrics of suction-feeding performance. We attempt to integrate a mechanistic view of the ability of fish to perform these components of suction feeding. We first discuss a model that successfully relates aspects of cranial morphology to the capacity to generate suction pressure in the buccal cavity. This model is a particularly valuable tool for studying the evolution of the feeding mechanism. Second, we illustrate the multidimensional nature of suction-feeding performance in a comparison of bluegill, Lepomis macrochirus, and largemouth bass, Micropterus salmoides, two species that represent opposite ends of the spectrum of performance in suction feeding. As anticipated, bluegills had greater accuracy, lower peak flux into the mouth, and higher flow velocity and acceleration of flow than did bass. While the differences between species in accuracy of strike and peak water flux were substantial, peak suction velocity and acceleration were only about 50% higher in bluegill, a relatively modest difference. However, a hydrodynamic model of the forces that suction feeders exert on their prey shows that this difference in velocity is amplified by a positive effect of the smaller mouth aperture of bluegill on force exerted on the prey. Our model indicates that the pressure gradient in front of a fish that is feeding by suction, associated with the gradient in water velocity, results in a force on the prey that is larger than drag or acceleration reaction. A smaller mouth aperture results in a steeper pressure gradient that exerts a greater force on the prey, even when other features of the suction flow are held constant. Our work shows that some aspects of suction-feeding performance can be determined from morphology, but that the complexity of the behavior requires a diversity of perspectives to be used in order to adequately characterize performance.

Mice homozygous for the scid mutation (scid mice) are severely deficient in functional B and T lymphocytes. The mutation appears to impair the recombination of antigen receptor genes and thereby causes an arrest in the early development of B and T lineage-committed cells; other hematopoietic cell types appear to develop and function normally. The arrest in lymphocyte development is not absolute; some young adult scid mice are "leaky" and generate a few clones of functional B and T cells. By 10-14 months of age, virtually all scid mice are leaky. Scid mice readily support normal lymphocyte differentiation and can be reconstituted with normal lymphocytes from other mice and even partially reconstituted with human lymphocytes. They also support the growth of allogeneic and xenogeneic tumors. Thus, scid mice are of interest for studies of both normal and abnormal lymphocyte development and function. In addition, they can be used to study the function of nonlymphoid cell types in the absence of lymphocytes.

Acipenseriformes (sturgeon and paddlefish) are basal actinopterygians with a highly derived cranial morphology that is characterized by an anatomical independence of the jaws from the neurocranium. We examined the morphological and kinematic basis of prey capture in the Acipenseriform fish Scaphirhynchus albus, the pallid sturgeon. Feeding pallid sturgeon were filmed in lateral and ventral views and movement of cranial elements was measured from video sequences. Sturgeon feed by creating an anterior to posterior wave of cranial expansion resulting in prey movement through the mouth. The kinematics of S. albus resemble those of other aquatic vertebrates: maximum hyoid depression follows maximum gape by an average of 15 ms and maximum opercular abduction follows maximum hyoid depression by an average of 57 ms. Neurocranial rotation was not a part of prey capture kinematics in S. albus, but was observed in another sturgeon species, Acipenser medirostris. Acipenseriformes have a novel jaw protrusion mechanism, which converts rostral rotation of the hyomandibula into ventral protrusion of the jaw joint. The relationship between jaw protrusion and jaw opening in sturgeon typically resembles that of elasmobranchs, with peak upper jaw protrusion occurring after peak gape.

The aim of this study was to investigate the function of the Hippo pathway member Yes-associated protein (Yap, gene name Yap1) in skeletal muscle fibres in vivo. Specifically we bred an inducible, skeletal muscle fibre-specific knock-in mouse model (MCK-tTA-hYAP1 S127A) to test whether the over expression of constitutively active Yap (hYAP1 S127A) is sufficient to drive muscle hypertrophy or stimulate changes in fibre type composition. Unexpectedly, after 5–7 weeks of constitutive hYAP1 S127A over expression, mice suddenly and rapidly lost 20–25% body weight and suffered from gait impairments and kyphosis. Skeletal muscles atrophied by 34–40% and the muscle fibre cross sectional area decreased by ≈40% when compared to control mice. Histological analysis revealed evidence of skeletal muscle degeneration and regeneration, necrotic fibres and a NADH-TR staining resembling centronuclear myopathy. In agreement with the histology, mRNA expression of markers of regenerative myogenesis (embryonic myosin heavy chain, Myf5, myogenin, Pax7) and muscle protein degradation (atrogin-1, MuRF1) were significantly elevated in muscles from transgenic mice versus control. No significant changes in fibre type composition were detected using ATPase staining. The phenotype was largely reversible, as a cessation of hYAP1 S127A expression rescued body and muscle weight, restored muscle morphology and prevented further pathological progression. To conclude, high Yap activity in muscle fibres does not induce fibre hypertrophy nor fibre type changes but instead results in a reversible atrophy and deterioration.

SUMMARYActivation and strain in the sternohyoideus (SH) were measured in vivo in five largemouth bass Micropterus salmoides. The SH is thought to actuate lower jaw depression, hyoid depression and suspensorial abduction during suction feeding in teleost fish. Sonomicrometry was used to measure fascicle shortening and lower jaw kinematics, while activity was measured by electromyography (EMG). SH fascicles shortened by an average of 11% during suction feeding. In three fish SH fascicles consistently shortened during fast lower jaw depression, but in two individuals they contracted isometrically or lengthened slightly during fast lower jaw depression. The SH continued shortening after peak gape, presumably actuating hyoid depression and lateral expansion of the buccal cavity. Onset of SH relengthening and onset of lower jaw elevation were simultaneous, as were the return of the SH to resting length and gape closure. Activation followed the onset of shortening by an average of 23 ms, although the muscle was active an average of 15 ms before the onset of rapid shortening. SH fascicles reached sustained shortening velocities averaging –2.5 fascicle lengths per second, and generally increased shortening velocity after peak gape. The shortening velocities measured in this study suggest that the SH actively shortens to generate power during suction feeding. This study is the first direct measurement of in vivo muscle function during suction feeding, the most common mechanism of prey capture among aquatic vertebrates.

Scid mice lack functional lymphocytes because they carry a mutation that impairs rearrangement of immunoglobulin and T-cell receptor (TCR) genes. Rearrangement of TCR ~, but not ~, and 13 genes, was routinely observed in DNA of scid thymocytes and thymocyte hybridomas. TCR 8 gene rearrangements appeared to involve DS1, D82, and JSl elements only; rearrangement of elements upstream of D~I (e.g., VS1) was not observed, and transcripts corresponding to fully assembled TCR 8 genes (VDJ8 or VDDJS) were not detected in RNA from scid thymocytes. These findings suggest that DS1, D82, and JS1 may be among the first TCR gene elements to undergo recombination and that scid T-lineage cells are developmentally arrested during or shortly after this stage of differentiation. One class of TCR 8 recombination fragments (D82-JS1) was amplified by the polymerase chain reaction (PCR) and cloned, and the recombination junctions were sequenced. Most fragments showed normal coding joints. Interestingly, five of seven coding joints that lacked N insertions showed evidence of recombination between short stretches (2-3 bp) of homologous sequence. As discussed, the general absence of VS-, J~/-, and ll3-associated rearrangements, despite the occurrence of normal D82-JS1 rearrangements, raises the possibility that the scid mutation may cause premature cessation of TCR gene recombination and thereby arrest early T-cell development.[Key Words: scid mice; T-cell receptor; T-cell development; polymerase chain reaction] Received January 14, 1991; revised version accepted May 17, 1991.Mice homozygous for the autosomal recessive mutation, scid (scid mice) are severely deficient in mature lymphocytes (Bosma et al. 1983). Early B-and T-lineage-committed cells are clearly present in scid lymphopoietic tissues but are unable to differentiate into functional B and T lymphocytes. This developmental arrest is believed to reflect a defect in the system responsible for the recombination of V (variable), D (diversity), and J (joining) gene elements that code for immunoglobulin and T-cell receptor (TCR) variable regions. Evidence of this defect is seen in rearranged immunoglobulin heavy-chain (IgH) genes of transformed scid pre-B cell lines (Schuler et al. 1986;Hendrickson et al. 1988;Kim et al. 1988;Malynn et al. 1988;Okazaki et al. 1988;Blackwell et al. 1989) and rearranged TCR ~/and genes of scid thymic lymphomas (Schuler et al. 1986(Schuler et al. , 1990. Most such rearranged genes show abnormal deletions of D-and J-or V-and J-coding elements, frequently extending 1 kb or more. In addition, transfection of transformed scid lymphocytes with extrachromosomal (Lieber et al. 1988) or retroviral recombination substrates (Ferrier et al. 1990;Hendrickson et al. 1990) has revealed a defect in the recombinase activity associated with VDJ 1Present address: Albany Medical College, Department of Microbiology and Immunology, Albany, New York 12208 USA. recombination: Although this activity can recognize, cleave, and join the recombination signal sequences that flank...