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#534783 05/05/21 10:06 AM
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I have a question for Ewest. I’ve been reading some older threads and I see in February 2015 you had an opinion that outbreeding depression could be caused as much by geography as by genetics. Maybe by stocking fish bred in one type of climate and taking them to a different climate. My question is in the last 6 years have you had a chance to gather new information on the subject and do you feel that it’s consistent with your theory?

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Alan not sure I understand the question. I have written a good bit on many subjects here on PB including outbreeding depression and other genetic topics. As best I can recall I have not seen any info connecting outbreeding depression with environment (location). However definitionally there is a connection (see red text in Wiki material at bottom). Outbreeding depression is a very complicated process and often with unknown cause. If you have a more specific question I will give it a shot - but often on PB the answer is "we just don't know".

A couple years back a group of us including Bob and Dr. Anderson , Bill C. and others discussed genetics vs adaptation (phenotypic plasticity) and time. It was used in a article Bob did on giant BG.

In that context genetics are very long term (we thought) and plasticity = adaptive behavior (adaptation) = phenotypic plasticity was short term changes due to environment. I have thought that phenotypic plasticity over the long term leads to genetic change. I have not seen that related to outbreeding depression which is genetic. For example the reduction in fitness in generations 2 onward in HBG .

I would be interested in seeing what I wrote on your question.

I am placing below an old PB article which might help with the concepts.

THE CUTTING EDGE – SCIENCE REVIEW
By Eric West

Young bluegill growth


Everyone who owns a pond or lake with fish has wondered what makes fish behave in certain ways. That question is often debated on the Pond Boss Forum and by anglers everywhere. The answers are often based on observation and experience which are in truth subject to all the human biases. In short there is a lot of disagreement on what makes fish grow and thrive. This applies not only to the casual observer or anglers but also to the scientists who study the what and why of fish behavior and how that affects growth. Is it hunger, fear, reproductive urges, anger , competition or other biological processes that control what fish do ? What part is based on instinct (genetics) and does conditioning play at part? All of this comes into context when we try to establish a bluegill or other forage base for a pond which will have bass or other high end predators. Early growth usually is the primary factor determining recruitment to age-1and thus establishment of a viable forge base.

Well with so much disagreement out there we may not get an iron clad answer but hopefully there will be some though provoking ideas. The authors of a recent study The Effect of Vegetation Density on Juvenile Bluegill Diet and Growth in the Journal of Freshwater Ecology 2012, 1–11 by Daniel E. Shoup , Michael A. Nannini & David H. Wahl discuss a number of their thoughts which are set out below.

At the start the authors noted that the role of vegetation density and its influence on juvenile bluegill diet and growth remains unclear. Even after the many studies that exist. They acknowledge much disagreement in the literature about how vegetation density affects foraging results and thus growth of juvenile bluegill. Several studies have found reduced foraging return for bluegill when they forage in structurally complex habitats, whereas others have found that bluegill growth was unaffected or even increased when foraging in complex environments. However these studies were with predators present. That is not the case when a typical bluegill or other forage base is first started in a new or renovated pond without predators.

In the Shoup et al study eight experimental 0.4-ha ponds (one acre with a mean depth of 1m) were used to evaluate the effects of habitat complexity on growth of small bluegill. Each pond was stocked with 15 kg of young-of-year bluegills (30–50 mm total length, approximately 20,000 fish per pond) to produce a realistic density for small ponds. The ponds contained varying amounts of vegetation (plants) and no predators.

The result was - by the end of the experiment, bluegill from the low vegetation treatment ponds were significantly longer – twenty (20%) percent than bluegill from the high vegetation treatment ponds. These results suggest that bluegill chose to forage in a vegetated habitat even in the absence of predation risk, resulting in reduced growth. The question is why and what caused the bluegill to stay and forage in the plants even when that was not optimum for growth and energy usage (energetics).

The difference in growth rates of bluegill in low and high vegetation density could be caused by several mechanisms. First, the high vegetation treatment may have had
lower prey abundance, and bluegill were unable to find sufficient food. However, this hypothesis does not appear likely as fish in both treatments appeared to find and ingest ample food resources. Mean stomach fullness values (1.4–4.3 mg dry prey/g wet predator) were higher than those reported for bluegill feeding in Lake Opinicon, Ontario. Stomach fullness was also similar to fish fed a 2.2% daily ration (g wet prey/g wet bluegill), the midpoint of the range of daily rations (1–4%) reported.

Also considered was that differences in energetic value or digestibility of the prey types eaten by fish in the two treatments may have differed. Bluegill in the high vegetation
treatment ingested more gastropods (snails) and odonates (dragon- and damselflies) and fewer chironomids (midges) than did the fish in low vegetation biomass treatment. However, all the commonly eaten prey types in this study have similar energy densities. No published information exists on the digestibility of these prey types to bluegill, but rainbow trout are able to assimilate similar amounts of energy from all three prey types. Therefore, it seems unlikely that energetic or digestibility differences among prey types could account for the difference in growth rate of bluegill between treatments.

Another noted possibility was that the potential difference in search efficiency or handling costs could account for the differences in growth rates between treatments. Bluegill that forage in vegetation expend more energy searching for prey. A consequence observed was while fish from both treatments had similar stomach fullness (suggesting similar consumption rates), it is likely that bluegill in the high vegetation treatment expended more energy to ingest their food, leading to reduced growth.

Regardless of the mechanism, the study results demonstrate that increased vegetation densities reduced bluegill growth rates even in the absence of pelagic (open-water) predation risk.

Diets of bluegill indicated that they fed mostly in littoral or benthic habitats.
Percent of pelagic zooplankton in the diet, excluding benthic ostracods (seed shrimp), was 51% by weight in both treatments. Although pelagic (open-water) zooplankton are often considered the optimal prey type for bluegill, several studies have demonstrated that bluegill eat a high proportion of macroinvertebrates (larger invertebrates) , presumably because they use littoral habitat to avoid predation risk associated with pelagic habitat . Similar predator-mediated habitat and diet shifts have been found for other fish species. Because piscivorous fish were not present in the study ponds used by Sloup et al, it was surprising that bluegill foraged so heavily in the vegetated habitat. Either bluegill cannot accurately assess predation risk or some other mechanism causes bluegill to forage in vegetated habitat. The propensity of bluegill to forage in vegetated habitat could be genetically linked or related to phenotype . In both cases, fish would not be expected to alter their habitat use in response to the absence of predators over short time scales. Bluegill may also select habitat due to temperature preference rather than foraging return highlighting the potential for mechanisms other than predation risk. Previous laboratory and enclosure studies have found that Eurasian perch (Perca fluviatilis) and roach (Rutilus rutilus) occasionally chose to feed in vegetation rather than open water even when no predator was present.

The authors’ bottom line - additional research is needed to determine the pervasiveness of these behaviors and the underlying mechanisms. Right back where we started – no iron clad answers but plenty to think about.

One area I wish the study would have addressed in more detail is phenotypic plasticity. That is the ability of an individual or population to change due to environmental influences. Can environmental conditions during early development shape individuals’ phenotypes so they become more adaptive to the conditions they encounter? Were the long bluegill that fed in open water that way because longer fish can swim better in open water and were the shorter bluegill that way because being short allows them to maneuver around the weeds better? Plasticity has been shown to effect sunfish (Lepomis) shape, feeding and behavior in some cases.

Might I suggest you help out your bluegill or other forage base fishes with supplemental feeding as it has been shown to be an efficient way to increase growth rates.

Here is stuff on the topic in general


From Wikipedia, the free encyclopedia

In biology, outbreeding depression is when crosses between two genetically distant groups or populations results in a reduction of fitness.[1] The concept is in contrast to inbreeding depression, although the two effects can occur simultaneously.[2] Outbreeding depression is a risk that sometimes limits the potential for genetic rescue or augmentations. Therefore it is important to consider the potential for outbreeding depression when crossing populations of a fragmented species.[1] It is considered postzygotic response because outbreeding depression is noted usually in the performance of the progeny.[3] Some common cases of outbreeding depression have arisen from crosses between different species or populations that exhibit fixed chromosomal differences.[1]

Outbreeding depression manifests in two ways:

Generating intermediate genotypes that are less fit than either parental form. For example, selection in one population might favor a large body size, whereas in another population small body size might be more advantageous, while individuals with intermediate body sizes are comparatively disadvantaged in both populations. As another example, in the Tatra Mountains, the introduction of ibex from the Middle East resulted in hybrids which produced calves at the coldest time of the year.[4]
Breakdown of biochemical or physiological compatibility. Within isolated breeding populations, alleles are selected in the context of the local genetic background. Because the same alleles may have rather different effects in different genetic backgrounds, this can result in different locally coadapted gene complexes. Outcrossing between individuals with differently adapted gene complexes can result in disruption of this selective advantage, resulting in a loss of fitness.


Mechanisms for generating outbreeding depression
The different mechanisms of outbreeding depression can operate at the same time. However, determining which mechanism is likely to occur in a particular population can be very difficult.

There are three main mechanisms for generating outbreeding depression:

Fixed chromosomal differences resulting in the partial or complete sterility of F1 hybrids.[1]
Adaptive differentiation among populations
Population bottlenecks and genetic drift

Some mechanisms may not appear until two or more generations later (F2 or greater),[5] when recombination has undermined vitality of positive epistasis. Hybrid vigor in the first generation can, in some circumstances, be strong enough to mask the effects of outbreeding depression. An example of this is that plant breeders will make F1 hybrids from purebred strains, which will improve the uniformity and vigor of the offspring, however the F2 generation are not used for further breeding because of unpredictable phenotypes in their offspring. Unless there is strong selective pressure, outbreeding depression can increase in further generations as coadapted gene complexes are broken apart without the forging of new coadapted gene complexes to take their place. If the outcrossing is limited and populations are large enough, selective pressure acting on each generation can restore fitness. Unless the F1 hybrid generation is sterile or very low fitness, selection will act in each generation using the increased diversity to adapt to the environment.[6] This can lead to recovery in fitness to baseline, and sometimes even greater fitness than original parental types in that environment.[7] However, as the hybrid population will likely to go through a decline in fitness for a few generations, they will need to persist long enough to allow selection to act before they can rebound.[8]

Examples
The first mechanism has the greatest effects on fitness for polyploids, an intermediate effect on translocations, and a modest effect on centric fusions and inversions.[1] Generally this mechanism will be more prevalent in the first generation (F1) after the initial outcrossing when most individuals are made up of the intermediate phenotype. An extreme case of this type of outbreeding depression is the sterility and other fitness-reducing effects often seen in interspecific hybrids (such as mules), which involves not only different alleles of the same gene but even different orthologous genes.

Examples of the second mechanism include stickleback fish, which developed benthic and lymnetic forms when separated. When crosses occurred between the two forms, there were low spawning rates. However, when the same forms mated with each other and no crossing occurred between lakes, the spawning rates were normal. This pattern has also been studied in Drosophilia and leaf beetles, where the F1 progeny and later progeny resulted in intermediate fitness between the two parents. This circumstance is more likely to happen and occurs more quickly with selection than genetic drift.[1]

For the third mechanism, examples include poison dart frogs, anole lizards, and ciclid fish. Selection over genetic drift seems to be the dominant mechanism for outbreeding depression.[1]
















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Sorry for the confusion ewest. I don’t know how to paste a thread. So I’m gonna give you the title of thread which is “ Bass Strains: Pro’s and Con’s?”. The date sent was 02/17/15 and the number was #401108. It ask for someone to point you to a study indicating outbreeding depression in Fla X Northern LMB in the zone where they occur naturally. It’s been six years since you wrote this thread and I am trying to find out if you have any new information on it.

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Understand now. That topic is still the same as far as I know. There are different opinions on the topic. My opinion is unchanged and I have seen no new data except as follows.

Is this the thread ? - https://forums.pondboss.com/ubbthreads.php?ubb=showflat&Number=401153&page=3

Here is one genetics study in TX (integrade zone) finding all types of Fla-Noth mixes and no mention of outbreeding issues.

https://forums.pondboss.com/ubbthre...ords=Carrillo&Search=true#Post529566

F1 LMB and Outbreeding Depression - Pond Boss Forum


[Linked Image]


Admixture Analysis of Florida Largemouth Bass and

Northern Largemouth Bass using Microsatellite Loci

DIJAR J. LUTZ-CARRILLO*

CHRIS C. NICE, TIMOTHY H. BONNER, AND MICHAEL R. J. FORSTN

LORAINE T. FRIES



Transactions of the American Fisheries Society 135:779�791, 2006

Copyright by the American Fisheries Society 2006



We found no evidence of a heterotic effect (in terms

of size) resulting from first-generation crosses between

Florida largemouth bass and northern largemouth bass.

The majority of trophy-sized fish with an admixed

genome were later-generation hybrids with a larger

percentage of Florida largemouth bass alleles. There

was also no observable negative impact on size from

the admixed genetic background in these fish, most

likely because of the modified environment to which

they were introduced and the nonadaptive radiation of

micropterids (Near et al. 2003).

Last edited by ewest; 05/05/21 02:28 PM.















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Yes, that’s the one thanks for the information. I’m gonna stay with my plans to stock 200 f1,100 fla., and 100 northern lmb. In my new pond. It’s about 8.5 acres. I put the BG, FHM, and GSH in last fall. I’ve got a lot of fry around the edges now IDK if there minnows or BG, but it’s a bunch. I got real good action at the feeders, so I think I’m ready for the bass.

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Are you stocking small 2-4 inch LMB ? If you are stocking larger LMB then reduce the # and wait until June.
















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Just called the fish farm and the supplier said his bass wouldn’t be ready before late July. He says they’ll be around 2” by July so I’ll be stocking fingerlings. My pond is creek fed and stays a cooler than a lot of ponds in my area so I guess they won’t get overly stressed. Plus the farm is only 2hrs away so not a long transport.


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